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E. R. Puppala et al.
234. Cherbut C, Michel C, Lecannu G. The prebiotic characteristics
of fructooligosaccharides are necessary for reduction of TNBSinduced colitis in rats. J Nutr. 2003;133(1):21–7.
235. Matsumoto S, Watanabe N, Imaoka A, Okabe Y. Preventive
effects of Bidobacterium- and Lactobacillus-fermented milk on
the development of inammatory bowel disease in senescenceaccelerated mouse P1/Yit strain mice. Digestion. 2001;64(2):92–9.
236. Gomollón F, Dignass A, Annese V, Tilg H, Van Assche G, Lindsay
JO, etal. 3rd European evidence-based consensus on the diagnosis
and management of Crohn’s disease 2016: part 1: diagnosis and
medical management. J Crohns Colitis. 2017;11(1):3–25.
237. Schultz M, Timmer A, Herfarth HH, Sartor RB, Vanderhoof JA,
Rath HC.Lactobacillus GG in inducing and maintaining remission of Crohn’s disease. BMC Gastroenterol. 2004;4:3–6.
238. Petersen AM, Mirsepasi H, Halkjær SI, Mortensen EM,
Nordgaard-Lassen I, Krogfelt KA. Ciprooxacin and probiotic
Escherichia coli Nissle add-on treatment in active ulcerative colitis: a double-blind randomized placebo controlled clinical trial. J
Crohns Colitis. 2014;8(11):1498–505.
239. Bourreille A, Cadiot G, Le Dreau G, Laharie D, Beaugerie L,
Dupas JL, etal. Saccharomyces boulardii does not prevent relapse
of crohn’s disease. Clin Gastroenterol Hepatol. 2013;11(8):982–7.
240. Guslandi M, Giollo P, Testoni PA.A pilot trial of Saccharomyces
boulardii in ulcerative colitis. Eur J Gastroenterol Hepatol.
2003;15(6):697–8.
241. Bousvaros A, Guandalini S, Baldassano RN, Botelho C, Evans
J, Ferry GD, etal. A randomized, double-blind trial of lactobacillus GG versus placebo in addition to standard maintenance
therapy for children with Crohn’s disease. Inamm Bowel Dis.
2005;11(9):833–9.
242. Prantera C, Scribano ML, Falasco G, Andreoli A, Luzi
C. Ineffectiveness of probiotics in preventing recurrence after
curative resection for Crohn’s disease: a randomised controlled
trial with Lactobacillus GG.Gut. 2002;51(3):405–9.
243. Zocco MA, Dal Verme LZ, Cremonini F, Piscaglia AC, Nista
EC, Candelli M, et al. Efcacy of Lactobacillus GG in maintaining remission of ulcerative colitis. Aliment Pharmacol Ther.
2006;23(11):1567–74.
244. Ishikawa H, Akedo I, Otani T, Umesaki Y, Tanaka R, Imaoka
A. Randomized controlled trial of the effect of bidobacteriafermented milk on ulcerative colitis. J Am Coll Nutr.
2003;22(1):56–63.
245. Triantafyllidi A, Xanthos T, Papalois A, Triantallidis JK.Herbal
and plant therapy in patients with inammatory bowel disease.
Ann Gastroenterol. 2015;28:210–20.
246. Park KT, Ehrlich OG, Allen JI, Meadows P, Szigethy EM,
Henrichsen K, etal. The cost of inammatory bowel disease: an
initiative from the Crohn’s & Colitis Foundation. Inamm Bowel
Dis. 2020;26(1):1–10.
247. Ordás I, Eckmann L, Talamini M, Baumgart DC, Sandborn
WJ. Ulcerative colitis. Lancet (London, England).
2012;380(9853):1606–19.
248. Knutson D, Greenberg G, Cronau H. Management of
Crohn’s disease—a practical approach. Am Fam Physician.
2003;68(4):707–14.
249. Rutgeerts P, Vermeire S, Van Assche G. Biological therapies for inammatory bowel diseases. Gastroenterology.
2009;136(4):1182–97.
250. Weisshof R, El Jurdi K, Zmeter N, Rubin DT.Emerging therapies
for inammatory bowel disease. Adv Ther. 2018;35(11):1746–62.
251. Chudy-Onwugaje KO, Christian KE, Farraye FA, Cross RK. A
state-of-the-art review of new and emerging therapies for the treatment of IBD.Inamm Bowel Dis. 2019;25(5):820–30.
252. Currò D, Ianiro G, Pecere S, Bibbò S, Cammarota G.Probiotics,
bre and herbal medicinal products for functional and inammatory bowel disorders. Br J Pharmacol. 2017;174(11):1426–49.
253. Hossen I, Hua W, Ting L, Mehmood A, Jingyi S, Duoxia X, etal.
Phytochemicals and inammatory bowel disease: a review. Crit
Rev Food Sci Nutr. 2020;60(8):1321–45.
254. Cirillo C, Capasso R. Constipation and botanical medicines: an
overview. Phytother Res. 2015;1493(10):1488–93.
255. Vezza T, Rodríguez-Nogales A, Algieri F, Utrilla MP, RodriguezCabezas ME, Galvez J. Flavonoids in inammatory bowel disease: a review. Nutrients. 2016;8(4):211.
256. Hoult JR, Payá M.Pharmacological and biochemical actions of
simple coumarins: natural products with therapeutic potential.
Gen Pharmacol. 1996;27(4):713–22.
257. Pithadia AB, Jain S. Treatment of inammatory bowel disease
(IBD). Pharmacol Rep. 2011;63(3):629–42.
258. Atreya I, Atreya R, Neurath MF. NF-kappaB in inammatory
bowel disease. J Intern Med. 2008;263(6):591–6.
259. Feng YJ, Li YY.The role of p38 mitogen-activated protein kinase
in the pathogenesis of inammatory bowel disease. J Dig Dis.
2011;12(5):327–32.
260. Broom OJ, Widjaya B, Troelsen J, Olsen J, Nielsen OH.Mitogen
activated protein kinases: a role in inammatory bowel disease?
Clin Exp Immunol. 2009;158(3):272–80.
261. Medina C, Radomski MW. Role of matrix metalloproteinases in intestinal inammation. J Pharmacol Exp Ther.
2006;318(3):933–8.
262. Langmead L, Makins RJ, Rampton DS.Anti-inammatory effects
of aloe vera gel in human colorectal mucosa in vitro. Aliment
Pharmacol Ther. 2004;19(5):521–7.
263. Zhu Q, Zheng P, Zhou J, Chen X, Feng Y, Wang W, et al.
Andrographolide affects Th1/Th2/Th17 responses of peripheral
blood mononuclear cells from ulcerative colitis patients. Mol Med
Rep. 2018;18(1):622–6.
264. Batiha GE-S, Olatunde A, El-Mleeh A, Hetta HF, Al-Rejaie
S, Alghamdi S, et al. Bioactive compounds, pharmacological
actions, and pharmacokinetics of wormwood (Artemisia absinthium). Antibiotics (Basel). 2020;9(6):353.
265. Kim H-J, Kim B, Lee M-R, Ra M, Lee Y.Bamboo shoot and artemisia capillaris extract mixture ameliorates dextran sodium sulfateinduced colitis. Curr Issues Mol Biol. 2022;44(10):5086–103.
266. Kiela PR, Midura AJ, Kuscuoglu N, Jolad SD, Sólyom AM,
Besselsen DG, etal. Effects of Boswellia serrata in mouse models of chemically induced colitis. Am J Physiol Gastrointest Liver
Physiol. 2005;288(4):G798–808.
267. Holleran G, Scaldaferri F, Gasbarrini A, Currò D.Herbal medicinal products for inammatory bowel disease: a focus on those
assessed in double-blind randomised controlled trials. Phytother
Res. 2020;34(1):77–93.
268. Hanai H, Sugimoto K. Curcumin has bright prospects for the
treatment of inammatory bowel disease. Curr Pharm Des.
2009;15(18):2087–94.
269. Bar-Sela G, Cohen M, Ben-Arye E, Epelbaum R.The medical use
of wheatgrass: review of the gap between basic and clinical applications. Mini Rev Med Chem. 2015;15(12):1002–10.
270. Zhou Y-H, Yu J-P, Liu Y-F, Teng X-J, Ming M, Lv P, etal. Effects
of Ginkgo biloba extract on inammatory mediators (SOD, MDA,
TNF-alpha, NF-kappaBp65, IL-6) in TNBS-induced colitis in
rats. Mediators Inamm. 2006;2006(5):92642.
271. Viladomiu M, Hontecillas R, Lu P, Bassaganya-Riera J.Preventive
and prophylactic mechanisms of action of pomegranate bioactive constituents. Evid Based Complementary Alternat Med.
2013;2013:789764.
272. Wang J, Zhang Z, Fang A, Wu K, Chen X, Wang G, et al.
Resveratrol attenuates inammatory bowel disease in mice by
regulating SUMO1. Biol Pharm Bull. 2020;43(3):450–7.
273. Wangchuk P, Navarro S, Shepherd C, Keller PA, Pyne SG, Loukas
A.Diterpenoid alkaloids of Aconitum laciniatum and mitigation

Herbal Medicines fortheManagement ofIrritable Bowel Syndrome andConstipation Problem
https://t.me/medicina_free
341
of inammation by 14-O-acetylneoline in a murine model of
ulcerative colitis. Sci Rep. 2015;5:12845.
274. Fernández-Bañares F, Hinojosa J, Sánchez-Lombraña JL, Navarro
E, Martínez-Salmerón JF, García-Pugés A, et al. Randomized
clinical trial of Plantago ovata seeds (dietary ber) as compared
with mesalamine in maintaining remission in ulcerative colitis.
Spanish Group for the Study of Crohn’s Disease and Ulcerative
Colitis (GETECCU). Am J Gastroenterol. 1999;94(2):427–33.
275. Chen C-L, Chen Y-P, Lin M-W, Huang Y-B, Chang F-R, Duh T-H,
etal. Euphol from Euphorbia tirucalli negatively modulates TGF-β
responsiveness via TGF-β receptor segregation inside membrane
rafts. PLoS One. 2015;10(10):e0140249.
276. Liu D-L, Li Y-J, Yang D-H, Wang C-R, Xu J, Yao N, et al.
Ganoderma lucidum derived ganoderenic acid B reverses ABCB1mediated multidrug resistance in HepG2/ADM cells. Int J Oncol.
2015;46(5):2029–38.
277. da Silva VC, de Araújo AA, de Souza Araújo DF, Souza Lima
MCJ, Vasconcelos RC, de Araújo Júnior RF, et al. Intestinal
anti-inammatory activity of the aqueous extract from ipomoea asarifolia in DNBS-induced colitis in rats. Int J Mol Sci.
2018;19(12):4016.
278. Lee S-J, Lee J, Song S, Lim K-T.Glycoprotein isolated from
Styrax japonica Siebold etal. Zuccarini inhibits oxidative and proinammatory responses in HCT116 colonic epithelial cells and
dextran sulfate sodium-treated ICR mice. Food Chem Toxicol.
2016;87:12–22.
279. Khare T, Palakurthi SS, Shah BM, Palakurthi S, Khare S.Natural
product-based nanomedicine in treatment of inammatory bowel
disease. Int J Mol Sci. 2020;21(11):3956.
280. Marius M, Amadou D, Donatien AA, Gilbert A, William YN, Rauf
K, etal. In vitro antioxidant, anti-inammatory, and invivo anticolitis effects of combretin A and combretin B on dextran sodium
sulfate-induced ulcerative colitis in mice. Gastroenterol Res Pract.
2020;2020:4253174.
281. Rong X, Ye CX.Simultaneous analysis of purine alkaloids and
catechins in Camellia sinensis, Camellia ptilophylla and Camellia
assamica var. kucha by HPLC.Food Chem. 2007;100:1132–6.
282. Vezza T, Rodríguez-Nogales A, Algieri F, Garrido-Mesa J,
Romero M, Sánchez M, etal. The metabolic and vascular protective effects of olive (Olea europaea L.) leaf extract in diet-induced
obesity in mice are related to the amelioration of gut microbiota
dysbiosis and to its immunomodulatory properties. Pharmacol
Res. 2019;150:104487.
283. Debnath T, Park P, Chandra N, Nath D, Binte N, Won H, etal.
Antioxidant activity of Gardenia jasminoides Ellis fruit extracts.
Food Chem. 2011;128(3):697–703. https://doi.org/10.1016/j.
foodchem.2011.03.090.
284. dos Reis SB, de Oliveira CC, Acedo SC, da Conceição Miranda
DD, Ribeiro ML, Pedrazzoli JJ, et al. Attenuation of colitis
injury in rats using Garcinia cambogia extract. Phytother Res.
2009;23(3):324–9.
285. Debnath T, Hasnat A, Pervin M, Lee SY, Park SR, Kim DH.Chaga
mushroom (Inonotus obliquus) grown on germinated brown rice
suppresses inammation associated with colitis in mice. Food Sci
Technol. 2012;21(5):1235–41.
286. Cho E, Shin J-S, Noh Y-S, Cho Y-W, Hong S-J, Park J-H, etal.
Anti-inammatory effects of methanol extract of Patrinia scabiosaefolia in mice with ulcerative colitis. J Ethnopharmacol.
2011;136(3):428–35.
287. Jin H, Lee B, Lim KJ, Debnath T, Shin HM, Lim BO. Antiinammatory effects of Prunus mume mixture in colitis induced
by dextran sodium sulfate. Korean J Med Crop Sci. 2011;19:1.
288. Fatani AJ, Alrojayee FS, Parmar MY, Abuohashish HM, Ahmed
MM, Al-Rejaie SS.Myrrh attenuates oxidative and inammatory
processes in acetic acid-induced ulcerative colitis. Exp Ther Med.
2016;12(2):730–8.
289. Fan F-Y, Sang L-X, Jiang M.Catechins and their therapeutic benets to inammatory bowel disease. Molecules. 2017;22(3):484.
290. Ye Z, Liu Z, Henderson A, Lee K, Hostetter J, Wannemuehler M,
etal. Increased CYP4B1 mRNA is associated with the inhibition
of dextran sulfate sodium-induced colitis by caffeic acid in mice.
Exp Biol Med (Maywood). 2009;234(6):605–16.
291. Abron JD, Singh NP, Price RL, Nagarkatti M, Nagarkatti PS,
Singh UP. Genistein induces macrophage polarization and systemic cytokine to ameliorate experimental colitis. PLoS One.
2018;13(7):e0199631.
292. Khan MS, Ikram M, Park JS, Park TJ, Kim MO.Gut microbiota,
its role in induction of Alzheimer’s disease pathology, and possible therapeutic interventions: special focus on anthocyanins.
Cells. 2020;9(4):853.
293. Zhang H, Zhuo S, Song D, Wang L, Gu J, Ma J, etal. Icariin inhibits intestinal inammation of DSS-induced colitis mice through
modulating intestinal ora abundance and modulating p-p65/p65
molecule. Turk J Gastroenterol. 2021;32(4):382–92.
294. Lin R, Piao M, Song Y. Dietary quercetin increases colonic
microbial diversity and attenuates colitis severity in citrobacter
rodentium- infected mice. Front Microbiol. 2019;10:1092.
295. Ai X-Y, Qin Y, Liu H-J, Cui Z-H, Li M, Yang J-H, etal. Apigenin
inhibits colonic inammation and tumorigenesis by suppressing
STAT3-NF-κB signaling. Oncotarget. 2017;8(59):100216–26.
296. Nunes C, Almeida L, Barbosa RM, Laranjinha J.Luteolin suppresses the JAK/STAT pathway in a cellular model of intestinal
inammation. Food Funct. 2017;8(1):387–96.
297. Medicherla K, Sahu BD, Kuncha M, Kumar JM, Sudhakar G,
Sistla R.Oral administration of geraniol ameliorates acute experimental murine colitis by inhibiting pro-inammatory cytokines
and NF-κB signaling. Food Funct. 2015;6(9):2984–95.
298. El Menyiy N, El Allam A, Aboulaghras S, Jaouadi I, Bakrim S,
El Omari N, et al. Inammatory auto-immune diseases of the
intestine and their management by natural bioactive compounds.
Biomed Pharmacother. 2022;151:113158.
299. Kudo T, Okamura S, Zhang Y, Masuo T, Mori M.Topical application of glycyrrhizin preparation ameliorates experimentally
induced colitis in rats. World J Gastroenterol. 2011;17(17):2223–8.
300. Lv J, Zhang Y, Tian Z, Liu F, Shi Y, Liu Y, etal. Astragalus polysaccharides protect against dextran sulfate sodium-induced colitis by
inhibiting NF-κВ activation. Int J Biol Macromol. 2017;98:723–9.
301. Nie Y, Lin Q, Luo F. Effects of non-starch polysaccharides on
inammatory bowel disease. Int J Mol Sci. 2017;18(7):1372.
302. Wen J-B, Zhu F-Q, Chen W-G, Jiang L-P, Chen J, Hu Z-P, etal.
Oxymatrine improves intestinal epithelial barrier function involving NF-κB-mediated signaling pathway in CCl4-induced cirrhotic
rats. PLoS One. 2014;9(8):e106082.
303. Nirmal SA, Ingale JM, Pattan SR, Bhawar SB. Amaranthus
roxburghianus root extract in combination with piperine as a
potential treatment of ulcerative colitis in mice. J Integr Med.
2013;11(3):206–12.
304. Zhang M, Long Y, Sun Y, Wang Y, Li Q, Wu H, etal. Evidence for
the complementary and synergistic effects of the three-alkaloid
combination regimen containing berberine, hypaconitine and skimmianine on the ulcerative colitis rats induced by trinitrobenzenesulfonic acid. Eur J Pharmacol. 2011;651(1–3):187–96.
305. Jiao Y-F, Lu M, Zhao Y-P, Liu N, Niu Y-T, Niu Y, et al.
N-methylcytisine ameliorates dextran-sulfate-sodium-induced
colitis in mice by inhibiting the inammatory response. Molecules.
2018;23(3):510.
306. Jiang Y, Zhao L, Chen Q, Zhou L. Exploring the mechanism of
berberine intervention in ulcerative colitis from the perspective
of inammation and immunity based on systemic pharmacology.
Evid Based Complement Alternat Med. 2021;2021:9970240.

342
https://t.me/medicina_free
E. R. Puppala et al.
307. Ghasemi-Pirbaluti M, Motaghi E, Naja A, Hosseini MJ. The
effect of theophylline on acetic acid induced ulcerative colitis in
rats. Biomed Pharmacother. 2017;90:153–9.
308. Niu X, Zhang H, Li W, Wang Y, Mu Q, Wang X, etal. Protective
effect of cavidine on acetic acid-induced murine colitis via regulating antioxidant, cytokine prole and NF-κB signal transduction
pathways. Chem Biol Interact. 2015;239:34–45.
309. Shirakami Y, Kochi T, Kubota M, Sakai H, Ibuka T, Yoshimi K,
etal. Inhibitory effects of pentoxifylline on inammation-related
tumorigenesis in rat colon. Oncotarget. 2018;9(74):33972–81.
310. Borniquel S, Jansson EA, Cole MP, Freeman BA, Lundberg
JO.Nitrated oleic acid up-regulates PPARgamma and attenuates
experimental inammatory bowel disease. Free Radic Biol Med.
2010;48(4):499–505.
311. Tyagi A, Kumar U, Reddy S, Santosh VS, Mohammed SB,
Ehtesham NZ, et al. Attenuation of colonic inammation by
partial replacement of dietary linoleic acid with α-linolenic
acid in a rat model of inammatory bowel disease. Br J Nutr.
2012;108(9):1612–22.
312. Sato K, Kanazawa A, Ota N, Nakamura T, Fujimoto K.Dietary
supplementation of catechins and alpha-tocopherol accelerates the
healing of trinitrobenzene sulfonic acid-induced ulcerative colitis
in rats. J Nutr Sci Vitaminol (Tokyo). 1998;44(6):769–78.
313. Motawea MH, Abd Elmaksoud HA, Elharrif MG, Desoky AAE,
Ibrahimi A.Evaluation of anti-inammatory and antioxidant prole of oleuropein in experimentally induced ulcerative colitis. Int
J Mol Cell Med. 2020;9(3):224–33.
314. Qian B, Wang C, Zeng Z, Ren Y, Li D, Song J-L.Ameliorative
effect of sinapic acid on dextran sodium sulfate-(DSS-)induced
ulcerative colitis in kunming (KM) mice. Oxid Med Cell Longev.
2020;2020:8393504.
315. Chen F, Liu Q, Xiong Y, Xu L.Current strategies and potential
prospects of nanomedicine-mediated therapy in inammatory
bowel disease. Int J Nanomedicine. 2021;16:4225–37.
316. Pita R, Ehmann F, Papaluca M. Nanomedicines in the
EU-regulatory overview. AAPS J. 2016;18(6):1576–82.
317. Rubino SJ, Selvanantham T, Girardin SE, Philpott DJ.Nod-like
receptors in the control of intestinal inammation. Curr Opin
Immunol. 2012;24(4):398–404.
318. Wang L, Yu M, Yang H.Recent progress in the diagnosis and precise nanocarrier-mediated therapy of inammatory bowel disease.
J Inamm Res. 2021;14:1701–16.
319. Yousef M, Pichyangkura R, Soodvilai S, Chatsudthipong V,
Muanprasat C. Chitosan oligosaccharide as potential therapy of
inammatory bowel disease: therapeutic efcacy and possible
mechanisms of action. Pharmacol Res. 2012;66(1):66–79.
320. Kanai T, Matsuoka K, Naganuma M, Hayashi A, Hisamatsu
T.Diet, microbiota, and inammatory bowel disease: lessons from
Japanese foods. Korean J Intern Med. 2014;29(4):409–15.
321. Olendzki B, Bucci V, Cawley C, Maserati R, McManus M,
Olednzki E, etal. Dietary manipulation of the gut microbiome in
inammatory bowel disease patients: pilot study. Gut Microbes.
2022;14(1):2046244.
322. Jang H-M, Kim J-K, Joo M-K, Shin Y-J, Lee K-E, Lee CK, etal.
Enterococcus faecium and Pediococcus acidilactici deteriorate
Enterobacteriaceae-induced depression and colitis in mice. Sci
Rep. 2022;12(1):9389.
323. Lee SH, Kwon JE, Cho M-L. Immunological pathogenesis of
inammatory bowel disease. Intest Res. 2018;16(1):26–42.
324. Li S, Wu B, Fu W, Reddivari L. The anti-inammatory effects
of dietary anthocyanins against ulcerative colitis. Int J Mol Sci.
2019;6:1–18.
325. Leccese G, Bibi A, Mazza S, Facciotti F, Caprioli F, Landini P,
et al. Probiotic Lactobacillus and Bidobacterium strains counteract adherent-invasive Escherichia coli (AIEC) virulence and
hamper IL-23/Th17 axis in ulcerative colitis, but not in Crohn’s
disease. Cells. 2020;9(8):1824.
326. Sivananthan K, Petersen AM.Review of Saccharomyces boulardii
as a treatment option in IBD.Immunopharmacol Immunotoxicol.
2018;40(6):465–75.
327. Zuo L, Yuan K-T, Yu L, Meng Q-H, Chung PC-K, Yang
D-H.Bidobacterium infantis attenuates colitis by regulating T cell
subset responses. World J Gastroenterol. 2014;20(48):18316–29.
328. Cheng F-S, Pan D, Chang B, Jiang M, Sang L-X.Probiotic mixture VSL#3: an overview of basic and clinical studies in chronic
diseases. World J Clin Cases. 2020;8(8):1361–84.
329. Shadnoush M, Shaker Hosseini R, Mehrabi Y, Delpisheh A,
Alipoor E, Faghfoori Z, etal. Probiotic yogurt affects pro- and
anti-inammatory factors in patients with inammatory bowel
disease. Iran J Pharm Res. 2013;12(4):929–36.
330. Zhang H, Duan Y, Cai F, Cao D, Wang L, Qiao Z, et al. Nextgeneration probiotics: microora intervention to human diseases.
Biomed Res Int. 2022;2022:5633403.
331. Ishisono K, Mano T, Yabe T, Kitaguchi K.Dietary ber pectin
ameliorates experimental colitis in a neutral sugar side chaindependent manner. Front Immunol. 2019;10:2979.

Herbal Medicines fortheManagement
https://t.me/medicina_free
ofDiseases onVitamin Deficiency
SathiSarkar, AnishKumarDas,
andSatheeshKumarNanjappan
Abstract
Vitamins are the key ingredients for the proper functioning of the body. Though it is needed in very small quantities, this does not reect their role. Except for some
vitamins, others will be obtained through diet. If the
required quantities are not met by the diet for a long time,
then deciency symptoms develop. Untreated deciency
symptoms progress to deciency disease or disorder,
which can result in death or a very unpleasant life. Herbal
remedies are the most ancient form of treatment. Most of
the old civilizations have their own natural treatment cultures. One of the most signicant advantages of these
herbal remedies is their chemical and biological diversities and negligible side effects. Considering these features, there is interest in shifting from synthetic medicine
to herbal or natural remedies. Many of the market surveys
show the prominent trend of this shift and predict this
natural product industry will be a $100 billion industry. In
this context, herbal remedies are also an alternative for
countering vitamin deciency and its symptoms. This
book chapter focuses on the available herbal remedies for
vitamin deciency. Along with that, we focus on the natural sources that contain the highest amount of respective
vitamins, which can be used for the future development of
herbal remedies, and we also raise awareness for the natural treatment of vitamin deciency. Plants and plantderived products are an important part of the human diet
and a major source of biologically active substances such
as vitamins, dietary bre, antioxidants, and cholesterollowering compounds. Though there is abundant information, plant nutrition has not been dened. Trial-and-error
methods were used to identify several plant nutrients and
health-promoting chemicals. Chromatography, mass
S. Sarkar · A. K. Das · S. K. Nanjappan (*)
Department of Natural Products, National Institute of
Pharmaceutical Education and Research (NIPER) - Kolkata,
Kolkata, West Bengal, India
e-mail: satheesh.niperk@nic.in
spectrometry, infrared spectroscopy, and nuclear magnetic resonance (NMR) allowed quantitative and qualitative analyses of plant metabolites around the turn of the
century. Plant biologists developed new techniques for
detecting and identifying phytochemicals. This section of
the chapter discusses the qualitative and quantitative procedures of vitamin analysis. We also discuss different
analytical approaches for the analysis.
Keywords
Vitamin deciency · Lifestyle diseases · Herbal
medicines
1 Introduction
Vitamins are a group of incredibly complicated organic molecules widely distributed in nature and absolutely required in
the human diet. It plays a signicant role in the human body’s
normal growth, development, and metabolism. Thirteen vitamins have been identied as essential to human nutrition and
have been split into two categories based on solubility [1].
Fat-soluble vitamins comprise vitamin A, vitamin D, vitamin
E, and vitamin K.Water-soluble vitamins comprise vitamin C
(ascorbic acid), vitamin B complex, as well as avonoids
(vitamin P) (Fig.1). Fat-soluble vitamins are related to fats
and are absorbed with dietary lipids. The fat-soluble vitamins
are absorbed in a similar way to the lipids. Water- soluble vitamins are not connected with fats and are unaffected by
changes in fat absorption [2]. The biological activity of various vitamins is linked to a group of structurally related molecules known as vitamers. In most situations, vitamers with
the same vitamin have similar qualitative biological attributes
to one another, but their potency varies due to tiny changes in
their chemical structures. Since the human body cannot synthesize vitamins, consuming them through diet is necessary.
Vitamin insufciency leads to severe or even deadly disorders. Vitamin deciency is linked to certain diseases, such as
vitamin A’s link to blindness, vitamin B1’s link to beriberi,
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. K. Dhara, S. C. Mandal (eds.), Role of Herbal Medicines, https://doi.org/10.1007/978-981-99-7703-1_17
343

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Fig. 1 Classication of
vitamins
S. Sarkar et al.
vitamin B3’s link to pellagra, vitamin B6’s link to anaemia,
vitamin C’s link to scurvy, and vitamin D’s link to rickets.
Thus, the deciency of vitamins affects the health and wellbeing of millions worldwide. The decit symptoms can also
be treated by replenishing these nutrients [3].
Throughout the history of civilization, herbal medicines
have been used to cure human ailments in every possible condition. Traditionally herbal medicine has been used in many
countries against various diseases. Ancient people believed in
and used plants and herbal remedies to heal illnesses. For primary health, 80% of the world’s demography depends on
herbal medicine [4]. Herbal medicines are natural products
that are isolated from plants. Natural products have attracted
interest over millions of years and are consequently being
used in modern medicine. Natural products have a wide
extent of chemical variety, i.e. they have multi- dimensional
structures, and hence biological activities are abundant.
Natural products play an increasingly important role as scientists continue to discover and rene new medications and lead
compounds through various approaches. Therefore, these
treatments have evolved from ancient or herbal therapies and
natural resources, 90–95% of drugs used to be made from
natural sources until high throughput screening was introduced to the drug discovery process [5]. Information on the
source of new drugs during 1981–2007 species that approximately 50% of the drugs are based on natural products [6]. As
herbal medicine contains naturally occurring bioactive constituents and nutritive substances, vitamin deciency disorders can be cured using herbal medicines.
2 Role ofVitamins intheBody
Vitamins have a crucial role in maintaining health, yet only a
tiny amount of them is required each day. Numerous cellular
processes rely on them, including cell division and development, but their primary job is converting food into usable
energy.
• Vitamin A helps teeth, bones, soft tissue, mucous mem-
branes, and skin grow and stay healthy.
• Vitamin D is called the “sunshine vitamin” because the
body makes it from sunlight. Most people at most latitudes need 10–15min of exposure 3 times a week to synthesize enough vitamin D.Sun-deprived people may not
produce enough vitamin D. Food alone cannot provide
enough vitamin D.Vitamin D absorbs calcium. Calcium
promotes healthy teeth and bones. It maintains calcium
and phosphorus blood levels.
• Tocopherol, or vitamin E, is an antioxidant. It helps in
vitamin K usage of the body and erythrocyte
production.
• Blood clots cannot form without vitamin K (coagulate).
There is evidence from scientic research that it benets
bone health.
• Vitamin C (Ascorbic acid) is an antioxidant that helps
keep teeth and gums healthy. It enables the body to take in
iron and keep its tissues healthy. It is also vital for healing
wounds.
• Thiamine (vitamin B1) helps the body’s cells turn carbs
into energy. Getting enough carbs is very important in
pregnancy or nursing conditions. It is also crucial for a
healthy heart and nerve cells.
• Riboavin (vitamin B2) helps the other B vitamins properly function in the body. It is also required for the growth
and formation of red blood cells.
• Niacin is a vitamin that keeps skin and nerves healthy. At
higher doses, it can also help lower cholesterol.
• Pantothenic acid (vitamin B5) is needed for the body to
break down food. It also has something to do with the
making of hormones and cholesterol.
• Vitamin B6 makes red blood cells and keeps the brain
running well. This vitamin is also an important part of the
proteins in the body, which are used in many chemical
reactions.
• Folate and vitamin B12 work together to help make red
blood cells. It is needed to make DNA, which controls
how tissues grow and how cells work. Folate is important
for any woman who is pregnant. Spina bida and other
birth defects can happen when there is not enough folate
in the body. Folate is now added to a lot of foods in the
form of folic acid [7].

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Fig. 2 Dietary sources of vitamins
3 Dietary Sources ofVitamins
Vitamins are considered “vital” since the body cannot produce them and must get them from the diet. Vitamin D boosts
calcium absorption, whereas iron absorption is enhanced by
vitamin C, and the B vitamins collaborate within cells. Most
vitamins need to be consumed consistently rather than stored
in the body, unlike vitamins A, E, and B12. Eating a variety
of foods from the four main food groups such as (1) vegetables and fruits, (2) grain foods, (3) milk and milk products,
and (4) legumes, nuts, seeds, sh and other seafood, eggs,
poultry and red meat with the fat removed will help to
achieve daily vitamin needs [8–10]. The dietary sources of
vitamins are shown in Fig.2.
4 Causes ofVitamin Deciency
Inappropriate eating habits often cause vitamin deciencies.
Vitamins are a range of complex compounds found in various plant and animal-based foods. The daily requirement of
vitamins is shown in Table1. There are multiple food sources
for each vitamin; some foods are fortied with vitamins.
Milk, for instance, has vitamin D added to it and naturally
Table 1 Vitamins and their required quantity
Required quantity
Men (intake per
Vitamins
Vitamin A
Thiamine (B1) 1mg 0.8mg
Riboavin (B2) 1.3mg 1.1mg
Niacin (B4) 16.5mg 13.2mg
Pantothenic acid
(B5)
Pyridoxine (B6) 1.4mg 1.2mg
Biotin (B7)
Folic acid (B9)
Cyanocobalamin
(B12)
Vitamin C 40mg
Vitamin D
Vitamin E 4mg 3mg
Vitamin K
day)
700μg 600μg
6mg 4mg
30μg 25μg
400μg
2μg
10μg
70μg 60μg
Women (intake per
day)
includes calcium (a mineral, not a vitamin). Numerous vitamins are typically added to cereal, rice, and pasta. While
proper vitamin intake from food sources is important,
absorption issues can also arise from medical problems.
Nutritional vitamin deciency can be caused by any or all of

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Fig. 3 Causes and symptoms of vitamin deciency
S. Sarkar et al.
the subsequent factors: inadequate consumption, poor
absorption, inadequate use, increased need, increased excretion, and increased degradation in the body. The causes and
symptoms of vitamin deciency are shown in Fig.3.
4.1 Dietary Risk Factors
Some eating plans are put at risk for vitamin deciencies.
Vegans and vegetarians are more likely to be decient in
vitamin B12 and biotin since these diets exclude animal
sources. There is a possibility of vitamin D deciency if
dairy products are avoided. Grain products, typically
enriched with vitamins in addition to their natural vitamin
content, are scarce in a gluten-free diet. As a result, maintaining a gluten-free diet might result in vitamin deciencies,
notably in B vitamins such as thiamine and folate. A lack of
vitamin E and K can occur on a diet high in processed foods
and low in fresh fruits and vegetables [11].
4.2 Sunlight
Foods, including seafood, eggs, and dairy products, are good
sources of vitamin D.Sun exposure can also provide vitamin
D.Vitamin D insufciency can be brought on by not getting
enough sun. Generally, this happens in the winter in areas
with a chilly environment [12].
4.3 Medical Illness
A range of diseases can hamper vitamin absorption and
metabolism. Vitamin deciencies typically result from various medical conditions, e.g. alcoholic liver disease, liver failure, kidney disease, chronic diarrhoea, malabsorption
syndrome, gastric bypass, inammatory bowel disease,
Crohn’s disease, irritable bowel syndrome, and pernicious
anaemia [13].
5 Symptoms ofVitamin Deciency
Symptoms of vitamin insufciency range from lethargy to
dry skin and hair to low mood to slow healing of wounds.
However, many of the symptoms shared by different decits
are similar. Most people exposed to low amounts for a while
will not see any visible signs until after a few months. The
causes and symptoms of vitamin deciency are shown in
Fig.3.
5.1 Fatigue andWeakness
Tiredness could be a sign of a vitamin D, B vitamin, or vitamin C deciency. If the body does not acquire enough vitamin D, bones and muscles may suffer, as well as fatigue and
weakness. Evidence links vitamin D deciency to weariness,

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and studies show that supplementing with vitamin D can
help treat this problem [14]. Anaemia, brought on by a lack
of folate, is a common cause of tiredness and weakness.
Because of a deciency in healthy red blood cells, oxygen
cannot be delivered to the body’s organs and tissues. The
body cannot function properly without oxygen, a vital energy
source [15].
5.2 Dry Skin andHair
Dry hair and cracked skin are common signs of vitamin A
deciency. Vitamins B, C, and D also show similar symptoms [16–18].
5.3 Depression
Vitamins B1, B3, B9, B12, vitamin C, and vitamin D deciencies can sometimes cause clinical depression [19–21].
5.4 Easy Bruising andBleeding
Easy bruising and bleeding can be caused by issues with
blood coagulation, sluggish healing, or collagen development. (Collagen strengthens the blood vessel wall.)
Signicant vitamin deciencies that can cause easy bruising
or bleeding are vitamin C and vitamin K (mainly in neonates) [22, 23].
5.5 Poor Wound Healing
In case of poor wound healing, sores take longer to cure.
Different vitamins, such as vitamins A, B, C, D, and K, are
helpful in this healing process. Some of them promote collagen formation, while others aid in the healing of certain
cell types or tissues and boost cellular health through the
antioxidant action [24, 25].
5.6 Predisposition toInfections
Deciency of some vitamins damages the system and can
make it more prone to infections and infectious disorders.
Examples of associated vitamins are—vitamins A, C, and D
[26, 27].
5.7 Bone Fracture
Bone health and strength depend on numerous vitamins,
including vitamins B6, B9, B12, C, D, and K.There is some
debate as to whether or not taking nutritional supplements
can reduce the incidence of fractures, even though evidence
shows the deciency of these vitamins can reduce bone density and eventually lead to fractures [28].
5.8 Skin Colour Changes
Loss of pigmentation in spots, hyperpigmentation, and overall pallor are probable outcomes of vitamin deciencyinduced alterations to the skin’s hue. Possible causes of
hypopigmentation and spotlightening include decits in vitamin D (in light-skinned people).
Darker pigmentation can be due to vitamin B12 and D (in
dark-skinned people). Deciencies that can cause generally
pale skin include vitamin C, vitamin B6, B9, and B12 [29].
Specic vitamin deciency diseases for each vitamin are
listed in Table2.
Table 2 Types of vitamin deciency diseases
Vitamin Deciency diseases
Vitamin A Night blindness, xeropthalmia,
keratomalacia
Vitamin D Rickets, osteomalacia
Vitamin E Neuromuscular, neurological disorders
Vitamin K Reduced blood clotting leading to
excessive bleeding
Vitamin B1 (Thiamin) Beri-beri
Vitamin B2 (Riboavin) Retarded growth, bad skin
Vitamin B3 (Niacin) Pellagra: dermatitis, dementia,
diarrhoea
Vitamin B5 (Pantothenic
acid)
Vitamin B6 (Pyridoxine) Anaemia
Vitamin B7 (Biotin) Alopecia and perioricial dermatitis
Folic acid Megaloblastic anaemia
Vitamin B12
(Cyanocobalamin)
Vitamin C Scurvy
Huntington’s disease
Pernicious anaemia

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6 Deciency Disorders ofVitamins
andTheir Herbal Remedies
6.1 Vitamin A
Vitamin A is a lipid-soluble compound that is a necessary
ingredient for human growth, survival, and the maintenance
of the immune system, eyesight, and eye health [30]. It is
available as a preformed vitamin (retinol) in dairy products,
eggs, meat, and sh liver oil like cod liver oil [31]. Provitamin
A or beta carotene is another vitamin A in dark green leafy
vegetables and deep orange fruits.
6.1.1 Deciency Disorders
Due to various causes, vitamin A deciency and overconsumption are common in society, with both conditions resulting in poor health. However, vitamin A insufciency is still a
signicant issue in South Asia and Africa, particularly among
preschool-age children and women of reproductive age, most
commonly at its nutritional deciency and its adverse health
consequences. The most severe clinical effects of vitamin A,
like corneal xerophthalmia, severe sickness, and mortality,
are most prevalent in older infants and young children of
6–59months. In all groups with vitamin A deciency, preventive supplementation should be given rst attention [32].
A lack of vitamin A results in ocular surface (OS) abnormalities such as severe dry eye disease (DED), corneal punctate keratopathy, and goblet cell loss that progresses until
they are absent. Extreme involvement causes keratinization
and epithelial metaplasia, leading to xerophthalmia (OS
keratinization with Bitot spots) and keratomalacia [33].
Xerophthalmia can also be directly caused by a vitamin A
decit. A condition in which the cornea swells up, the conjunctiva (the eye’s covering) dries up, and the eyes get ulcerated, known as dry eye disease. Although the cause was
unknown, early civilizations’ records and traditions indicated that eating animals and sh livers had healing properties. Vitamin A should consequently be administered to
everyone who has xerophthalmia.
6.1.2 Herbal Medicine forVitamin ADeciency
6.1.2.1 Antioxidants
Night blindness, cataract, and glaucoma can all be treated
with herbal remedies. Since oxidative stress plays a crucial
role in the pathogenesis of several common eye ailments,
numerous studies have proven that herbal medications
include a variety of antioxidants that may be effective for eye
protection.
6.1.2.2 Carotenoids
The xanthophyll family of carotenoids, which includes lutein
and zeaxanthin, is frequently found in tomatoes, Chinese
wolfberries, and carrots. Additionally, lutein protects the
retina from the oxidative stress brought on by diabetes [34].
6.1.2.3 Omega 3 Fatty Acid
Since oxidative stress has a major role in the pathogenesis of
numerous common eye ailments, several studies have proven
that herbal medications include a variety of antioxidants that
may be effective for eye protection, which are essential fatty
acids, crucial for maintaining good health. However since
the body cannot synthesize them, they must be consumed
through diet. Algal oil, axseed oil, and sea buckthorn seed
are typical plant sources [35]. Numerous studies have been
conducted on these omega-3 fatty acids’ role in maintaining
eye health.
6.2 Vitamin D
The fat-soluble vitamin 1a-25-dihydroxyvitamin D3 (vitamin D) is essential for human health and plays a role in bone
metabolism, immunological function, and calcium homeostasis. Vitamin D is abundant in sh liver oils and several
saltwater species, including herring, salmon, and sardines.
The food chains from plankton are likely the source of the
vitamin D found in sh liver.
6.2.1 Deciency Disorders
Two metabolic bone illnesses, i.e. osteomalacia in adults and
rickets in children, are known to be triggered by a lack of
vitamin D [36]. Vitamin D insufciency correlates to various
chronic medical disorders, including osteoporosis, myopathy, lung illness, increased inammation, and lowered immunity [37].
The lack of vitamin D has also been related to several
cardiovascular risk factors [15]. Vitamin D deciency can
increase the generation of reactive oxygen species and the G
protein RhoA by boosting the synthesis of renin and angiotensin II. Insulin resistance and metabolic syndrome are
brought about by inhibiting intracellular glucose transporter
pathways [17]. A typical ricket symptom is decreased Ca and
P in the organic matrix of bone and cartilage. Since all three
nutrients are essential for healthy bone production, the indications and symptoms are identical to those of a deciency
of Ca, P, or both. Osteoporosis is characterized by a loss in
bone mass that can cause fractures with just minor damage.
Rickets is caused by improper growth plate mineralization

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and is almost always found in developing youngsters. On the
other hand, osteomalacia is caused by improper mineralization of the prefabricated osteoid and occurs in both adults
and children in addition to rickets [36, 38]. When the bone
mass is too low, skeletal integrity and mechanical support
can no longer be preserved, and fractures can happen with
little to no damage.
There are three different types of treatment for vitamin D
deciency: supplementation, natural ultraviolet B radiation,
and sunshine. Every form of treatment has potential drawbacks and advantages [39]. Based on these ndings, foods
like milk and butter are now irradiated with UV light to
increase their vitamin D content, and so help eliminate rickets as a major health problem around the world.
6.2.2 Herbal Medicine forVitamin D Deciency
For osteomalacia and rickets, Bladderwrack (Fucus vesiculosis) is used. Comfrey decoction and tincture Calendula
(Marigold) are also used to treat osteomalacia and rickets. As
an alternative to Comfrey, fenugreek seeds might be utilized.
Fenugreek and St John’s Wort tablets and capsules benet
from treating osteomalacia and rickets. Herbs like
Chamomile, Dandelion, Clivers, Horsetail, Meadowsweet,
Coltsfoot, Mistletoe, Plantain, Scarlet Pimpernel, Silverweed,
Toadax, and Shepherd’s Purse can be consumed as teas,
powders, tablets, or capsules. A herbal combination of
Comfrey, Horsetail, Kelp, Lobelia, Marshmallow root, Oats,
and Parsley root can also be used for the treatment. Along
with this, exposure to sunlight is a supportive treatment
option for vitamin D deciency disease [40]. Osteomalacia
is also treated using tablets or capsules prepared from
Bamboo gum, Black Cohosh, Echinacea, Kelp, and Prickly
Ash.
6.3 Vitamin E
Different lipid soluble components were rst identied in
1922 by Evans and Bishop and were later grouped under the
label “vitamin E” [41]. The vitamin E group together, known
as chroman-6-ols or tocochromanols, is divided into tocopherols (α, β, γ, and δ tocopherols) and tocotrienols (α, β, γ, and
δ tocopherols) that are present in food containing vitamin E
as a whole [42]. Plants synthesize tocopherol and tocotrienol
from homogentisic acid. Only α tocopherol satises the
human vitamin E needs, even though these forms have antioxidant properties but cannot be transformed into one
another [43]. Vegetable oils are one of the primary dietary
sources of vitamin E.Vitamin E may also be found in nuts in
reasonable amounts. For instance, vitamin α T is primarily
present in peanuts, almonds, and sunower seeds, whereas
vitamin γ T is the main vitamin E in walnuts, pecans, pistachios, and sesame seeds [44, 45]. Compared to other oils,
soybean, sunower, maize, walnut, cottonseed, palm, and
wheat germ oils have comparatively greater vitamin E concentrations (more than 50mg of vitamin E/100g oil) [43,
46].
For a diet high in vitamin E to work well, it must also be
abundant in foods high in these other nutrients. α-Tocopherol
is the predominant form of vitamin E in the circulation,
although γ-tocopherol is consumed in relatively higher
amounts from the diet than α-tocopherol due to the preferential binding afnity of the α-tocopherol transfer protein
(α-TTP) for tocopherol. Transfer of α-tocopherol to the
plasma membrane involves α-TTP [47].
In order to prevent lipid peroxidation and shield cell
membranes from oxidative damage, vitamin E is the rst line
of defence [48]. Different experiment reports show that a
combination of tocopherols had a higher inhibitory impact
than alpha-tocopherol alone on lipid peroxidation in human
erythrocytes. Its ability to scavenge peroxyl radicals also
safeguards the polyunsaturated fatty acids in plasma lipoproteins and membrane phospholipids [49]. It has been discovered that although gamma-tocopherol captures and
neutralizes the existing free radicals, the production of new
free radicals is mainly prevented by alpha-tocopherol.
Several ailments and diseases, including cancer, ageing,
arthritis, and cataracts, have been related to oxidation. As a
result, vitamin E may aid in the prevention or postponement
of chronic disorders caused by reactive oxygen species
molecules.
It has been discovered that elevating the level of alphatocopherol in endothelial cells prevents platelet aggregation
and causes the endothelium to produce prostacyclin. This
impact was brought on by the dysregulation of the vascular
cell adhesion molecule (VCAM-1) and the intracellular cell
adhesion molecule (ICAM-1), which reduced the adherence
of blood cell constituents to the endothelium. Additionally,
when vitamin E activates cytosolic phospholipase A2 [50]
and cyclooxygenase 1 [51] in the arachidonic acid cascade,
more prostacyclin is released, which acts as a signicant
vasodilator and inhibitor of platelet aggregation in humans
[52]. Protein phosphatase 2A is activated by vitamin E,
which increases PKC-dephosphorylation and reduces protein kinase C (PKC) activity. Vitamin E has also been shown
to inhibit PKC in a number of different cell types, which has
been shown to inhibit platelet aggregation, reduce the proliferation of monocytes, macrophages, neutrophils, and vascular smooth muscle cells, and reduce the production of
superoxide in neutrophils and macrophages [42, 53].
6.3.1 Deciency Disorders
Vitamin E insufciency creates a specic neurological illness. It typically results from malabsorption aggravating
chronic cholestasis, abetalipoproteinemia, celiac disease, or
cystic brosis [54]. Malabsorption is a common cause of
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