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3.4.3 Vicenin-2
Vicenin-2 (VCN-2), a avonoid glycoside with the chemical
name apigenin-6, is 8-di-C-D-glucopyranoside. The ethnopharmacological sources include Cyclopia subternata and
Perilla frutescens. Studies have demonstrated the antidiabetic, antioxidant, antiglycation, anti-inammatory, antithrombotic, and antiplatelet properties of VCN-2. VCN-2
post-treatment signicantly reduces the activation of MAPK,
such as ERK, JNK, and p38, indicating that VCN-2 prevents
sepsis by preventing MAPK signalling. VCN-2 represents a
possible pharmaceutical strategy to prevent liver failure by
attenuating liver damage by suppressing TLR signalling
[118]. By suppressing the protein tyrosine kinase Src and
activating the protein tyrosine phosphatase SHP-1, VCN-2
efciently reduced both constitutive and induced STAT3
phosphorylation. JAK protein, which controls STAT3
upstream activity, was suppressed by VCN-2 [119]. Proinammatory mediators, like IL-6 and TNF-α, are downregulated by VCN-2, which directly responsible for
pro-inammatory responses, such as leukocyte adherence,
permeability, and migration towards endothelial cells.
VCN-2 might prevent NF-κB activation [120].
3.4.4 Schaftoside
Schaftoside (SFS) is an active phytoconstituent of the
Chinese herb Herba Desmodii Styracifolii. SFS exhibits
many potent pharmacological activities, including inammatory inhibition, anti-hepatitis, anticancer, etc. SFS also
has a vital role in regulating liver cirrhosis and lipid homeostasis [121].SFS promoted lipolysisin Huh-7 cells, resulting in the downregulation of TG and LDL-C, which
eventuallydecreasedliver steatosis. In addition, SFS could
inhibit SREBP-1c expression, reducing HFD-induced elevations in hepatic TG level, suppressing lipid droplet formation, and ameliorating HFD-induced liver injury [122]. At
both the mRNA and protein levels, SFS reduced the
lipopolysaccharide- enhanced upregulation of ATF4 (activating transcription factor 4), XBP-1 (X-box-binding protein-1), and CHOP (C/EBP homologous protein) [123].
3.4.5 Geniposide
Geniposide (GPS) is the major active phytochemical of
Gardenia jasminoides Ellis and having the molecular formula of C17H24O
GPS is an example of an iridoid glycoside
10.
[124]. Numerous pharmacologic actions of this active phytochemical include anti-inammatory analgesic, hepatoprotective, and choleretic properties. CGA and GPS treat fatty liver
disease by reducing the fat content upregulated by free fatty
acids (FFAs) in HepG2 cells [125]. GPS-mediated preventative action is maintained by downregulating TC, TG, and
LDL-C levels and increasing HDL-C biosynthesis. GPS
increased insulin levels and decreased FFA levels, suggesting that it may be a possible treatment for preventing high-
fat- diet-induced hepatic steatosis. GPS upregulates PPAR-α
expression and downregulates TNF-α. This indicated that
GPS modulation of lipid metabolism could be associated
with PPAR-α expression and adipocytokine release. GPS
signicantly decreased GSH-Px and SOD, reduced MDA,
and lowered CYP2E1 activity. The antioxidant activity of
GPS might be explained by its capacity to inhibit the production of free radicals or by its free radical scavenging activity
[126].
3.4.6 Swertiamarin
Enicostemma littorale Blume, a member of the Gentianaceae
family, is the major source of swertiamarin (SWT). SWT is a
seco-iridoid glycoside type of phytochemical. SWT has been
discovered to have benecial effects, including analgesic,
hepatoprotective, antidiabetic, and gastroprotective effects
[127]. Hepatic SOD, GPx, CAT, GST, and GSH activities
were all signicantly reduced by CCl4 treatment. SWT signicantly improved the levels of GSH and the activity of
those antioxidant enzymes in the liver of CCl4-treated rats. It
was proposed that SWT might reduce oxidative stress by
restoring the activity of antioxidant enzymes and elevating
the level of GSH in the liver, at least in part. In addition,
SWT signicantly lowered levels of inammatory cytokines
(IL-1β, IL-6, and TNF-α), which reduced inammatory
response. In animals with acute cirrhosis, the concentrations
of both total CYP and CYP isoenzymes were shown to be
lower. Due to oxidative stress, the primary liver P450 isoenzymes, CYP2C6, CYP1A2, CYP2E1, and CYP3A2, and
their protein expression, drastically decreased in activity
during acute liver damage brought on by CCl4 treatment
[128]. Revealed SWT could accelerate the healing of CCl4induced liver damage by recovering hepatic CYP3A and
CYP2E1 expression. Treatment with SWT also restored
NQO1 expression that CCl4 had downregulated. These ndings suggested that the upregulation of NQO1 and HO-1 and
the Nrf2 pathway activation may be related to SWT hepatoprotective properties [129]. SWT treatment successfully
decreased the expression of SREBP-1, ACC, and FAS, suggesting that the drug suppressed DNL through its impact on
these regulating elements. By controlling RAS, SWT has the
potential to be an effective treatment for hepatic brosis
[130].
3.4.7 Salidroside
Salidroside (SDS) is a phenolic glycoside having the chemical name [2-(4-hydroxyphenyl) ethyl-beta-D-glucoside].
SDS is commonly present in Rhodiola sacinehalnsis.
Ligustrum lucidum has recently been discovered to have a
signicant level of SDS.SDS showed several pharmacological effects, including hepatoprotective, neuroprotection, free
radical scavenging, immunological modulation, and kidney
protection [131]. SDS might be used to treat NAFLD because
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it can inhibit the deposition of lipids in muscle and liver tissues by stimulating AMPK activity. SDS can treat NAFLD,
which works by controlling the AMPK-dependent NLRP3/
TXNIP pathway and oxidative stress [132]. It was found that
SDS effectively lowered ALT and AST levels in the serum in
CCl4-induced hepatic brosis mice. Still, it was also found
to prevent the liver tissue, demonstrating that SDS could
lessen the damage caused by inammation in the progression of liver brosis. Sphingosine kinase 1 (SphK1) suppression signicantly lowered the degree of liver brosis,
whereas high levels of SphK1 expression have also been
seen to promote the advancement of liver brosis. Conversely,
levels of SphK2 are lower in alcoholic-induced cirrhosis and
hepatocellular carcinoma in livers. Research showed that
SDS might reverse these modications, whether helpful or
harmful [133]. Table4 includes biological role offew glycosides involved in recovering cirrhosis andvarious chronic
liver ailments.
3.5 Terpenoids
The two most signicant categories of plant secondary
metabolites are terpenes and terpenoids. They are hardly
ever linked to hepatoprotective effects. Terpenoids exhibit
hepatoprotection by suppressing apoptosis in liver cells by
limiting the release of cytochrome c from the cytoplasm,
lowering the Bax/Bcl-2 ratio, and blocking the phosphorylation of JNK and ERK. Terpenoids comprise extracts with
strong radical-scavenging properties that can boost the overall antioxidant capability and lessen hepatitis-related inammation. By modifying the activity of cytochrome P450
enzymes, they play a signicant part in the biotransformation of xenobiotics. In-depth explanations are provided for
other effects, including regulating TGF-β stimulated collagen type I production linked to liver brosis and the specic
actions of certain terpenoids [138]. Some potent terpenoids
have been depicted in Fig. 6 and described below in
detail(Table 5).
3.5.1 Betulinic Acid
Betulinic acid (BLA) is a cyclic triterpene in several plants,
including Betula. By altering the AMPK-SREBP signalling
pathway, BLA signicantly lowered hepatic fat buildup
[139]. BLA activates calmodulin-dependent protein kinase
to activate AMPK.Additionally, BLA inhibits the expression
of S6 kinase-mediated SREBP1. Treatment with BLA blocks
the effects of the HFD on the activation of nuclear SREBP1
and the subsequent buildup of TG in the liver [140].
3.5.2 Ursolic Acid
Ursolic acid (URA), a natural terpenoid, is the main active
component of many traditional medicinal plants, including
Cornus ofcinalis. URA has been implicated in various biological activities, such as lipid regulation, glucose metabolisms, and anti-atherosclerotic [141]. URA-fed mice had
much smaller and lighter adipose tissues than the high-fat
diet controls due to a decrease in lipid formation in adipose
tissue. The main mechanisms by which URA exerts its hypolipidemic effects are the activation of PPAR and the management of its responsive genes involved in fatty acid and
lipoprotein metabolism [142]. URA may have triggered
endogenous ligand production or increased the availability
of endogenous ligands through indirect methods to activate
PPAR.After URA administration, the expression of PPAR
and its responsive genes in lipid metabolism was dramatically altered in the liver by regulating the CPT1 and ACOX1
genes. In addition, SREBP1, FAS, and SCD1 gene expression levels were suppressed by URA administration, which
decreased the production of hepato-fatty acids and reduced
TG levels in the blood [143].
3.5.3 Artemisinin
Artemisia annua L. is the source of numerous terpenoidbased bioactive phytochemicals. The antimalarial drug artemisinin (ATM) is one of those. Hepatic ACC levels were
signicantly greater in Artemisia annua L. extract-fed animals. By administering artemisia extract, HFD-induced
nuclear ChREBP and SREBP1 expression were considerably reduced. The extract dramatically reduced HMGB1
expression. RAGE expression was not signicantly reduced
by ATM treatment in the HFD-fed mice, though. The use of
ATM signicantly reduced COX-2 levels as well. The treatment of Artemisia annua extracts also reduced CTGF and
TGF-β1 levels [144].
3.5.4 Oleanolic Acid
Oleanolic acid (OLA) is a triterpenoid isolated from Olea
ferruginea, which grows in Kashmir, India. Numerous plant
species worldwide also contain OLA, including Eugenia
jambolana, Tiarella polyphylla, Clerodendrum spicatum,
Olea europaea, etc. OLA is a very potent phytochemical that
exhibits a wide range of biological actions [145]. The administration of OLA restored the levels of hepatotoxic blood
marker enzymes and showed a substantial protective impact
on ethanol-induced liver injury. The elevated level of CCL4induced blood hepatic enzymes signicantly decreased
OLA.OLA reversed the elevated levels of MDA and reduced
the activity of SOD and GPx [146]. The liver lipid levels
progressively recovered to normal after OLA administration,
while ALT and AST levels were markedly lowered. OLA
decreased the upregulation of IL-6, IL-1β, and TNF-α and
the production of pro-inammatory factors in HFD mice. In
liver tissues, OLA dramatically reduced the phosphorylation
and degradation of IκB-α and p65-induced nuclear translocation [147].
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[134]
[126]
[135]
[136]
[137]
Didymin decreased ERS, ROS, Bax, GRP78, XBP1 ATF6 cytochrome c, and
caspase-9 enhanced the expressions of CAT, GSH, and SOD, Bcl-2
GPS caused increased expression of PPAR-α, SOD, and GSH-Px, HDL-C
activity, and decreased MDA, CYP2E1, TG, TC, and LDL-C activity
Gentiopicroside inhibited protein and mRNA expression of α-SMA and
collagen I in TGF-β-activated LX-2 cells. Decreased SREBP1 and increased
AMPKα, PPAR-α and phosphorylated ACC
20±2g)
rats, 200±20g.
Animal experiment male
C57BL/6 mice (8–10weeks,
20–22g)
manshurica Kitagawa
Diosgenin Inhibits the expression of α-SMA and TGF-β. In addition, it
inhibited the TGF-β1-induced expression of collagen I and α-SMA in HSC-T6
cells
mRNAs encoding DGATs and GPAT, and increases serum and hepatic TG
levels. In addition, tectoridin signicantly elevated the content of GSH and the
activities of GSH-Px and SOD
In vitro, the human HSC cell
line, HSC-T6
In vitro male C57BL/6 mice Tectoridin causes a reduction of serum ALT and AST levels, expression of
species
lobata
Compound name Biological source Research model Biomarkers Refs.
Didymin Origanum vulgare L. Male C57BL/6J mice (SPF,
Table 4 Names, biological sources, experiment research models, and targeted biomarkers of glycosides
GPS Gardenia jasminoides In vitro male Sprague-Dawley
Gentiopicroside Roots of Gentiana
Diosgenin Solanum and Dioscorea
Tectoridin The ower of Pueraria
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Fig. 6 Terpenoids in the treatment of liver cirrhosis
3.5.5 Lycopene
Lycopene (LYP) is present in many natural plants and food
sources. LYP is primarily found in red-coloured vegetables
and fruits, including tomatoes, pink guavas, watermelons,
and apricots [148]. Pretreatment with LYP revealed that
LYP could prevent the changes in ALT and AST, lower TC,
TG, LDL-C, and FFA levels, and raise HDL-C.In addition, LYP elevated SOD and GSH and decreased MDA
activities against NAFLD, indicating that the activity of
antioxidants may be involved in the mechanism of its hepatoprotective effects. In contrast, animals on HFD had a
substantial downregulation of CYP2E1 expression after
receiving the LYP treatment [149]. LYP inhibited NF-κB
activation and decreased interleukin IL-6, IL-1β, and
TNF-α levels. The liver antioxidant enzymes GPx, SOD,
and CAT were enhanced by LYP. LYP suppressed HSC
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[159]
[160]
the inammatory mediators like NF-κB, COX-2, iNOS and
B-cryptoxanthin restraining M1 or M2 activation of liver
pro-inammatory cytokines (TNF-α, IL-6, MCP-1, and IL-1β)
[161, 162]
macrophages/Kupffer cells. Reductions in serum levels of MDA,
hs-CRP, IL-6, and CK18-M65
Downregulation of CYP2C, TNF-α, SREBP-1c, IL-1β, FAS,
MCP1, SCD1, α-SMA, CD36, IRS1, FOXO1, AKT, and GSK3β
erythropoietin, ME1 and CCND1 and upregulating the expression
of IPP, HMGCS, FDPS, CXCL1, C4BP, CYP7A1, A2M, TFRC,
[163, 164]
FLT1, (PSMB 10, NQ01) and p53 signalling gene (TNFRSF6,
FAS)
Downregulated α-SMA, TGF-β1, NF-κB, IL-6, IL-1β, TXNIP,
GPx, while upregulated GSH, Nrf2, HO-1, and p53
) adults
2
Wistar rats weighing 150–200g Downregulated ALT, AST, LDH, and ALP in ALD, downregulating
In vitro human voluntary overweight/
obese (25≤BMI <40kg/m
(18≤age<60years)
In vitro HepG2 (p53 positive) human
such as kale and spinach
Green and yellow vegetables
and algae
liver cancer cells and female Sprague-
Dawley rats, 56-week old
Cimicifuga racemosa (L)
Nutt.
C57BL/6 mice and in vitro HepG2 cells
Compound name Biological source Research model Biomarkers Refs.
Lutein Dark green leafy vegetables,
Table 5 Names, biological sources, experiment research models, and targeted biomarkers of terpenoid
Β-cryptoxanthin
Actein Actaea racemosa L. syn. And
Andrographolide Andrographis paniculata In vitro CCl4-induced liver brosis male
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activation, and cellular lipid storage was altered. LYC
treatment increased PPAR-α along with PPAR-β and
PPAR-γ expressions of retinoid X receptor [150].
3.5.6 Fucoxanthin
A naturally occurring, low molecular weight, and chemically
active carotenoid, fucoxanthin (FXN) is primarily generated
from several marine algae. FXN concentration in seven
microalgae isolates was measured, and the Synuroceae family had abundant FXN.The microalgae Tisochrysis lutea can
also produce a high yield of FXN [151]. Dietary FXN signicantly reduced the liver mRNA expression of brotic
genes such as Timp1, collagen type I alpha 1 chain (Col1α1),
and TGF-β1. As an indicator of activated HSCs, αSMA
mRNA and protein expression were decreased by FXN.These
ndings imply that dietary FXN inhibits the progression of
brosis by controlling the expression of brogenic factors
[152]. In LX-2 cells, FXN suppressed the basal and TGF-β1induced mRNA and protein expression of pro-brogenic
genes by dramatically inhibiting SMAD3 activation. The
TGF-1 signalling pathway, which is implicated in the onset
of liver brosis, must include SMAD3. FXN markedly
decreased both baseline and TGF-β1-induced TIMP1 expression. Its inhibitory effects on ROS buildup likely inuence
the anti-brogenic actions of FXN through decreasing NOX4
expression and on TGF-triggered suppression of PPAR-γ
[153]. FXN inhibited lipid accumulation by suppressing the
expression of lipogenesis and β-oxidation, including adipose
TG lipase, phosphorylated hormone-sensitive lipase, PPAR,
CPT1, CPT2, and upregulating the expression of genes
involved in lipolysis and β-oxidation [154].
3.5.7 Tanshinone IIA
One of the main lipophilic substances obtained from Salvia
miltiorrhiza root and the extract is tanshinone IIA (TIIA)
[155].TIIA has a variety of biological actions, including the
ability to protect against liver damage, hepatic steatosis, liver
cirrhosis, hepatic brosis, and HCC [156]. The high levels of
AST, ALT, ALP and TBIL in serum and of Hyp in hepatic
tissue can be dramatically reduced by TIIA.TIIA can signicantly lessen liver brosis, collagen deposition in hepatic tissue, and liver damage. TIIA successfully reduced the two
markers (α-SMA and COL1A2) in vivo. MMP9, c-Jun,
PI3K, c-Myc, and P38 could target genes for TIIA, and all
these proteins were increased in CCl4-induced liver brosis.
In TGF-treated LX2 cells, TIIA signicantly reduced the
expression of c-Jun, MMP9, c-Myc, CCND1, P-P65, PI3K,
and P38. TIIA may reduce liver brosis through various targets and signalling pathways, and it can shed light on the
pharmacological processes by which it works to treat hepatic
brosis [157]. It is commonly accepted that the excess deposition of ECM proteins is a key component of hepatic brosis. The extensive synthesis and secretion of ECM are
controlled by activated α-SMA and HSCs, and COL1A2 are
molecular indicators of HSC activity. TIIA markedly downregulated the protein expression of these genes’ products.
TIIA therapy reduced ECM synthesis (COL1A2), HSC proliferation, and α-SMA expression, reducing the activation of
HSC-LX2 cells [158].
3.6 Tannins
Tannins are sophisticated polyphenolic substances found in a
wide variety of plants, particularly vascular plants. Tannin
can capture free radicals. In addition, tannins have a hydroxyl
group and a conjugated double bond (Fig.7) that allow the
electron to delocalize, making them particularly efcient as
an electron/hydrogen atom donor and chelating metal [165].
3.6.1 Tannic Acid
Tannic acid (TNA) is a hydrolysable tannin polyphenol produced by plants. It is a gallic acid polymer glucoside that
may be found in a variety of dietary plant products, including
sorghum grain, coffee, tea, and cocoa [166]. NAFLD development is signicantly inuenced by ChREBP, the transcriptional activator of lipogenic genes. Through acetylation of
Lys-672, p300 raises ChREBP transcriptional activity, which
raises p300 occupancy on target gene promoters. Additionally,
NAFLD is brought on by p300 overexpression. Histone acetyltransferases and histon deacetylases (HDACs) control the
typical epigenetic process known as histone acetylation.
Cancer, inammation, and metabolic problems are linked to
an imbalance between HAT and HDAC activity [167]. TNAinduced suppression of HAT activity reduces the development of NAFLD pathological characteristics. TNA prevented
p300 from occupying the promoters of FAS and ATP-citrate
lyase sterol regulatory element, ultimately leading to the
hypoacetylation of H3K9 and H3K36. TNA also reduced the
acetylation of total proteins and the histone H3 protein at
lysine residues 9 and 36. Through these mechanisms, TNA
suppressed the in vivo accumulation of fat by lowering the
mRNA expression of genes essential for lipogenesis [168].
3.6.2 Dieckol
Dieckol (DCK) is a phlorotannin found in Ecklonia cava.
Phlorotannin is a group of substances having polymerized
phloroglucinol units. DCK from Laminaria japonica reduces
hepatic steatosis by enhancing hepatic fatty acid β-oxidation
[Liu Y etal., 2019]. The impacts of DCK on NAFLD might
be made by reducing the development of the NLRP3 inammation and pyroptosis in aHFD-induced mice NAFLD
model, HFD considerably enhanced food intake and weight
changes, but DCK treatment markedly reduced them. HFD
also raised the blood levels of LDL and total cholesterol,
which were then decreased by DCK [169]. HFD enhanced
HO
HO
OH
Dieckol
OH
Punicalagin
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OH
O
HO
HO
HO
OH
O
O
OH
O
O
O
HO
OH
O
OO
O
OH
Tannic acid
O
O
OO
O
O
OH
OH
O
OH
OH
OH
OH
O
OH
HO
HO
HO
HO
HO
O
O
HO
O
Corilagin
HO
O
O
OH
O
O
O
OH
O
O
HO
OH
O
OH
OH
OH
OH
O
O
O
OH
OH
HO
OH
OH
OH
OH
HO OH
O
O
HO OH
OH
Fig. 7 Terpenoids in the treatment of liver cirrhosis
OH
OHO
O
OO
OH
OH
M1 inltration but reduced M2 inltration in the lymphatic
vasculature of the liver. DCK treatment resulted in a decrease
in M1 inltration and an increase in M2 inltration. HFD
induced an uptick in IL-6 and TNF-α expression in the liver,
while DCK treatment had the opposite effect. HFD lowered
the expression of VEGFC and VEGFR3, whereas DCK treatment increased it. When mice were given the HFD, the
expression of the lymphangiogenesis-related PI3K, pAKT,
and pERK signalling pathways dropped, while DCK
increased it [170]. With the administration of DCK, high-fat
died induced lipogenic genes (FASN, SREBP2, and FABP4)
expressions were signicantly reduced. High-fat diet ele-
HO
O
O
O
O
OH
HO
O
O
OH
OH
OH
OH
O
O
HO
O
OHO
HO
OH
HO
HO
vated TLR4 and NF-κB expression in the liver. DCK downregulates the overexpression. When DCK was administered,
the NLRP3 inammasome’s elements, such as ASC and
NLRP3, were reduced in the liver of HFD animals. In the
liver, HFD raised the ratio of cleaved-caspase-1 to caspase-1,
whereas DCK treatment lowered it [171].
3.6.3 Corilagin
Corilagin (CRL) is a gallotannin, one of the main active phytochemicals in various ethnopharmacological plants, including Phyllanthus emblica, Phyllanthus reticulatus,
Dimocarpus longan, and Geranium wilfordii. According to
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reports, CRL exhibits many pharmacological properties,
such as anti-tumour, antioxidant, hepatoprotective, and antiinammatory properties [172]. CRL reduced the severity of
GalN/LPS-induced liver damage by regulating oxidative
stress and inhibiting apoptosis. CRL prevented the development of schistosomiasis-affected hepatic brosis by inhibiting the miR-21/SMAD7/ERK pathway [173]. The hepatitis
C virus (HCV) NS3 serine protease, a well-known target for
preventing HCV replication, was demonstrated to be inhibited by CRL.CRL therapy may signicantly alter the gene
expression patterns in the liver brought on by a high-fat diet.
High plasma ALT and AST values are two well-known biomarkers of hepatocellular damage. CRL effectively prevented the HFD-induced rise in ALT and AST levels in
plasma, demonstrating its protective effects on liver function
in developing NAFLD. CRL treatment in HFD-fed mice
resulted in better plasma lipid proles caused by NAFLD.It
lowers levels of TG, TC, and LDL-C as well as higher levels
of HDL-C.CRL downregulated Hsd3b5 expression, which
may have contributed to its inhibitory effect on the development of NAFLD [174].
3.6.4 Punicalagin
Punicalagin (PCG) is a well-known phytochemical in pomegranate (Punica granatum L.) peel. Being used primarily in
Asian nations for traditional medicine, it is currently widely
grown in Southwest America, California, Mexico, and
Africa. It has a variety of pharmacological properties, such
as antioxidant, anti-atherosclerotic, hepatoprotective, and
hypolipidemic properties, that have been reported [175].
PCG enhanced the adipokine pathway and reduced oxidative
stress in eWAT (epididymal white adipose tissue), which
improved lipid homeostasis in the liver and adipose tissue.
When mice were given a western diet, PCG reduced the
number of hepatic lipids [176]. In addition, PCG could shield
rats from cyclophosphamide-induced liver toxicity. PCG
reduced the levels of TNF-α, NF-κB, p65, IL-1β, inducible
nitric oxide synthase, and caspases 3 and 9 to prevent
cyclophosphamide- induced liver inammation and death
[177]. By decreasing the production of ROS and NO and
raising the expression of SOD1, PCG prevented the oxidative stress caused by lipopolysaccharides (LPS) in macrophages. PCG activated the Nrf2-signalling pathway to
signicantly reduce the effects of FFA-induced lipotoxicity
in HepG2 cells. PCG therapy decreased the MDA level and
upregulated SOD and GPx activities against CCL4-induced
liver injury [178].
4 Conclusion
Unhealthy dietand alcoholism are thetwo factorsprimarily
bring on cirrhosis. DNL causes hindrance of lipid metabolism, which accelerates oxidative stress to promote lipid
accumulation and inammation in healthy hepatocytes.Naturally obtained compounds work as boons in treating these complicated diseases, while synthetic medications
leave adverse imprints. Currently, herbal medicines are trying to be clinically reused like traditional medicines concomitantly with synthetic ones. The search for suitable natural
products for complicated diseases stands as a gold mine for
medical research. SMR, hesperidin, CUR, etc., have already
shown good hepatoprotective properties and are viable therapy alternatives on their own or as a supplement when taken
with other medications. Undoubtedly, there is a great potential for natural substances to be effective options for liver
cirrhosis. Therefore, we expect that the study on the pathophysiology of hepatic injuries and progression to cirrhosis
and future therapeutic medication development for cirrhosis
and associated liver conditions may be theoretically supported by the information in this chapter.
Funding None.
Conict of Interest The authors declare no conicts of
interest.
Acknowledgement All the authors acknowledge the Department of
Pharmaceutical Technology, Jadavpur University, Kolkata, for providing research amenities.
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