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18
Role of phytopharmaceuticals in
inflammatory disorders
US Mahadeva Rao
1
, Jamal Basa Dudekula
3
,
Shvetank Bhatt
4
, M. Sathish Kumar
3
, Kamal Shah
5
,
Nagendra Singh Chauhan
6
and Satish Shilpi
2, 3
1
School of Basic Medical Science, Faculty of Medicine, Universiti Sultan Zainal Abidin, Kuala
Terengganu, Malaysia;
2
Department of Pharmaceutics, Faculty of Pharmacy, DIT University,
Dehradun, Uttarakhand, India;
3
Amity Institute of Pharmacy, Amity University Madhya
Pradesh, Gwalior, Madhya Pradesh, India;
4
Department of Pharmacology, School of Pharmacy,
MIT World Peace University, Pune, Maharashtra, India;
5
Institute of Pharmaceutical Research,
GLA University, Mathura, Uttar Pradesh, India;
6
Drugs Testing Laboratory, Avam
Anusandhan Kendra (State Government Lab of AYUSH), Raipur, Chhattisgarh, India
1. Introduction
Innate imm unity serves as the body’s first line of defense and is nonspecific[1]. It gener-
ates both cytokines and chemokines, which activate the immune system quickly and attract
immunoglobulin to the inflammatory region [2,3]. Effective phagocytosis serves as the first
line of defense against antigens and is carried out by neutrophils and macrophages [3,4].
The pathogen-identifying APCs use their surface-expressed sequence identifying receptors
to attach strongly to the sequence of the molecules formed with microorganism cells mem-
brane [5]. After phagocytosis, antigen-presenting macrophages deliver major histocompati-
bility complexes (MHCs) and antigenic peptides produced from the ingested pathogen to
the surface of immune cells. CD4þ Complicated class II encompasses adaptive immunity
involving T-lymphocyte [6,7], after which, it liberates additional proinflammatory cytokines,
including Tumor Necrosis Factor-a, IL-6 and 12, and interferons-I and II. All of these coop-
erate to eradicate the infection as members of the adaptive immune response.
Vasodilation brough t on by the production of histamine, prostaglandins (PGs), and nitric
oxide (NO), which increases blood circulation as well as the leukocyte level, is the primary
CHAPTER
433
Phytopharmaceuticals and Herbal Drugs
https://doi.org/10.1016/B978-0-323-99125-4.00002-0 © 2023 Elsevier Inc. All rights reserved.
https://t.me/med1917
source of inflammatory responses [8]. Furthermore, leukocyte vascular permeability is
elevated by proinflammatory cytokines like tumor necrosis factor-alpha (TNF-),
interleukin-1 (IL-1), and interleukin-6 (IL-6) produced by activated immune cells by
improving leukocytes concentration on endothelial [9,10]. Howeve r, chronic inflammation
can result in serious problems such as it disturbs the metabolic process of cells, and inducing
false proteolysis which leads to apoptosis. It develops the condition of tissue malfunction
[10]. Inflammation is often induced to restore homeostasis and heal tissues. Inflammatory ab-
normalities have been connected to epigenetic alterations in numerous recent studies [10].
One of the following categories best describes medications used to treat inflammatory
disorders.
1. First-line antihistamine drugs
2. Broad-spectrum medications, such as steroidal antiinflammatory medications (SAMe),
and nonsteroidal antiinflammatory drugs (NSAIDs) (glucocorticoids)
3. Medicines meant to combat a particular disease and used to treat ailments like gout,
skin problems, and asthma
Besides other apparent changes like increased capillary permeability and a build-up of in-
flammatory cells at the site of injury, tissue damage causes local blood vessels to enlarge. A
crucial part of the beginning of the inflammatory process is played by leukocytes. While lym-
phocytes, basophils, and eosinophils are typically linked to specific, more chronic types of in-
flammatory reactions, neutrophils and macrophages are principally responsible for acute and
nonspecificinflammation. Normal circumstance s result in localized, transient inflammation
that resolves on its own [11,12]. Different studies reveal various aspects of innate immunity,
inflammation, and the connection between TLR4 signaling, inflammatory diseases, and can-
cer. The current review highlights recent findings in targeted phytotherapy and depends on
the several authoritarian aspects connected to inflammation. Since ancient times, phytochem-
icals produced from plants have been used as a primary and supplementary therapy for a
wide range of disorders that affect cell functioning. Phytochemical-mediated therapies
have lately attracted a lot of interest to retard inflammatory syndrome and chronic illnesses
such as cancer; diabetes; cardiovascular, hepatic, and neurological disorders. Protein kinases,
redox status, inflammatory transcription factors, cytokines, and enzymes that generally pro-
mote inflammation are only a few of the cell signaling pathways that are modulated by phy-
tochemicals to have antiinflammatory effects.
2. Antiinflammatory phytochemicals
Phytochemicals are chemicals obtained from natural sources that are beneficial to human
wellness [13]. Flavonoids and tannins, glucosinolates, alkaloids, and terpenoids are examples
of the bioactive compounds found in nature (Table 18.1)[14], which have an impact on a va-
riety of natural processes of signaling in humans [15e18]. Many inflammatory diseases are
now being treated with natural products, which are becoming mo re and more accepted
[19,20]. It is fascinating that most of the herbal extracts having antiinflammatory activity
were found to have an impact on important TLR4 signaling and repolarization of the macro-
phage [21].
18. Role of phytop harmaceuticals in inflammatory disorders434
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TABLE 18.1 Antiinflammatory phytoconstituents.
S.
No. Phytoconstituent Nature Source
1 Resveratrol Phenolic stilbene
derivative
Peanuts, berries, and grape skins
2 Curcumin Polyphenol is usually
found in nature
Turmeric (curcuma longa
3 Quercetin Flavonoid Lemon, orange, apples, grapes
Genistein Isoflavonoid Red clover, legumes, and soy-based diets
5 Sodium butyrate Butyrate Beans, peas, and soybeans
6 Glycyrrhizinate, diammonium
glycyrrhizinate
Saponin Licorice
7 Proanthocyanidins Polyphenols Cranberry, blueberry, and grape seeds
8 Bromelain Enzymes Pineapple
9 Naringenin Flavonoid Citrus fruit
10 Naringin Flavonoid Citrus fruits
11 Chrysin Flavonoid Propolis, honey, and passion fruit
12 Mangiferin Glucoside Mangifera indica plant
13 Lupeol Triterpenoid Cabbage, green pepper, grapes strawberry, olive,
mangoes and
14 Bauerenol Triterpenoid Indian suregada angustifolia
15 Ficusogenin Triterpenoid Constituents of the leaves of ficus carica
16 Capsaicin Neuropeptide Capsicum
17 Anthocyanins Flavonoid Berries, currants, grapes
18 Myricetin Flavonoid Berries, tea
19 Galangin Flavonol Alpinia officinarum (lesser galangal)
20 Fisetin Flavonol Strawberry, apple, persimmon
21 Apigenin Flavone Chamomile tea
22 Luteolin Flavonoid Plant reseda luteola
23 Catechin Flavonoids Mimosa catechu
24 Epigallocatechin Polyphenol Teas, cranberries, strawberries, blackberries,
kiwis, cherries
25 Lycopene Carotenoid Tomatoes carrots, watermelons, grapefruits, and
papayas
26 Peonidin Cyanidin Grapes, blueberries, cherries
27 Cyanidin Grapes, blueberries, cherries
28 Malvidin Flavonoids Blueberries, pomegranates, and strawberries
29 Lutein Carotenoids Kale, parsley, spinach, broccoli, and peas
30 Astaxanthin Carotenoids Algae, yeast, salmon, trout, krill, shrimp, and
crayfish
31 a-Carotene, b-carotene Terpenoids Carrots, spinach, lettuce, tomatoes
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3. Phytopharmaceuticals regulate inflammatory markers and thus boost
immunity to alleviate COVID-19 (SARS-CoV-2)
3.1 Cytokine storm
The WHO declared SARS-CoV-2 a pandemic in March 2020. Pneumonia and ARDS are
caused by the coronavirus which belongs to the Coronaviridae family. The virus is spread
by coming into contact with aerosol droplets from infected people. The pathogenesis of
SARS-CoV-2 is quite complex and includes the override of the host’s innate and antiviral de-
fenses, induction of oxidative stress, and hyper inflammation known as the “cytokine storm,”
which results in pneumonia, tissue fibrosis, and severe lung injury.
Numerous vaccines and medications are currently being evaluated for their efficacy,
safety, and ability to determine SARS-CoV-2 dosages; this requires a significant amount of
time for their authentication. Therefore, investigating the repurposing of natural substances
may offer solutions to treat SARS-CoV-2. Numerous dietary supplements have been shown
to have immune-stimulating, antiviral, anti-FRSA, and antiinflammatory activities. These
include lactoferrin, quercetin, probiotics, selenium, zinc, calciferol, ascorbic acid, curcumin,
cinnamaldehyde, and ascorbic acid.
The appropriate mix of some of these nutraceuticals in the form of a dietary supplement
may assist to support this condition both prophylactically and therapeutically by enhancing
the immune system, preventing virus outbreaks, preventing infection from progressing to an
awful level, and further suppressing hyperinflammation.
In vitro anti-COVID-19 properties of various phenolic natural compounds were examined
by Orfalie et al. [22]. They discovered that sinapic acid (SA) can prevent the growth of virus
in vitro with an IC50 value of 2.69 g/mL, and it was further confirmed by a modest cytotox-
icity assay (CC50 ¼ 189.3 g/mL). Additionally, a link between the FRSA, polyphenol concen-
tration, cytotoxic action, and the suppression of proinflammatory cytokines appeared to exist.
This study suggests that sinapic acid is a potential structural pattern for the creation of anti-
SARS CoV-2 agents [23].
4. Resveratrol
A phytoalexin called resveratrol (RES, 3, 4
0
, 5-trihydroxystilbene) provides protective ac-
tion against plant diseases. Resveratrol is a naturally occurring phenolic stilbene derivative.
It can be found in peanuts, berries, and grape skins [24]. Both the trans- and cis-isoforms of
this phenolic molecule occur, albeit the trans-isoform is more stable [25 ]. It prevents RAW
264.7 macrophages that have been stimulated from expressing TLR4 and MyD88 [26]. The
systemic circulation quickly absorbs and breaks down resveratrol. According to a study,
resveratrol has antiinflammatory and tissue-protective properties. In A549 cell lines, resver-
atrol blocks the manufacturing of IL-8 and also stops the creation of granulocyte-
macrophage colony-sti mulating factors. For the treatment of inflamma tory illnesses, it acts
as a choice of drug related to other nonsteroidal antiinflammatory drugs (Fig. 18.1)[27].
It blocks the transcription factors NF-kB, MAPK, IRF-3, and AP-1 as well as the enzymes
iNOS, COX-2, and 5-LOX [28,29]. It suppresses the NF-kB-induced formation of free radicals
18. Role of phytop harmaceuticals in inflammatory disorders436
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like NO and ROS, LTs, and PGs, as well as proinflammatory cytokines including TNF-a, IL-6,
and IL-1b [30,31]. It blocks TLR4/NF-kB signaling and lowers myocardial TNF-a production
in a rat heart model with ischemic injury.
5. Curcumin
Curcumin (CUR) is a polyphenol usually found in nature. Turmeric (Curcuma longa)isa
yellow pigment made from a flowering plant in the ginger family [32]. It stops lipid perox-
idation and lysosomal enzymes from developing [33,34]. An experiment on cell lines sup-
ports curcumin’s antiinflammatory properties (BV-2 microglial cells). The use of curcumin
was observed to diminish the expression of COX-2 receptors and the secretion of inflamma-
tory factors like TNF-, PGE, and nitric oxide from cells. According to repo rts, curcumin’s
bioavailability was found to enhance when combined with piperine. It demonstrated the anti-
inflammatory and antioxidant benefits of both animal and human models (Fig. 18.2) [35].
Curcumin is a polyphenolic antiinflammatory active constituent of turmeric utilized to
treat and manage different metabolic disorders and illnesses, such as arthritis. In a study,
it was fo und that curcumin reduces the chances of arthritis. It was also found that sustained
release formulation can provide a better antiinflammatory effect in comparison to plain cur-
cumin in case of arthritis. It was confirmed by the reduced level of neutrophils and leuko-
cytes, TNFa, IL-1, and 6. The study concluded that the encapsulated curcumin showed a
better antiinflammatory effect in comparison to plain curcumin [36].
Heidari-Beni et al. [37] developed a formulation with hydroalcoholic extract of turmeric
and administere d it to patients having osteoarthritis disease, which found a significant reduc-
tion in inflammatory factors. Comparatively, it showed a similar result which was found with
a therapeutic dose of diclofenac. In comparison with diclofenac, curcumin does not precipi-
tate any side effects. In a randomized study design, three groups had 15 rheumatoid arthritis
patients administered 500 mg of curcumin for the first group, 50 mg of diclofenac for the
FIGURE 18.1 Resveratrol.
FIGURE 18.2 Curcumin.
5. Curcumin 437
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