Green tea polyphenol epigallocatechin-3-gallate inhibits oxidative damage and preventive effects on carbon tetrachloride–induced hepatic fibrosis

Mao, Zhen; Wang, Qian; Huang, Xiaohui; Cao, Liangqi; Chen, Xiling; Sun, Kai; Liu, Yunjian; Li, Wen; Zhang, Longjuan

doi:10.1016/j.jnutbio.2006.12.016

Cited by 92 publications

(59 citation statements)

References 44 publications

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“…More importantly, the model has been useful in evaluating hepatoprotective potential of various natural and synthetic compounds (Ahmad et al, 2009;George & Chandrakasan, 2000;Wang et al, 2012;Zhen et al, 2007). In the present study, we have demonstrated the efficacy of vitamin B 12 in alleviating NDMA-induced intensive fibrosis in rats.…”

Section: Discussionsupporting

confidence: 52%

Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Ahmad

Afroz

Gupta

et al. 2014

Pharmaceutical Biology

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Context: Altered vitamin B 12 levels have been correlated with hepatotoxicity; however, further evidence is required to establish its protective role. Objective: To evaluate the effects of vitamin B 12 supplement in protecting N 0 -nitrosodimethylamine (NDMA)-induced hepatic fibrosis in Wistar rats. Materials and methods: Hepatic fibrosis was induced by administering NDMA in doses of 10 mg/kg body weight thrice a week for 21 days. Another group received equal doses (10 mg/kg body weight) of vitamin B 12 subsequent to NDMA treatment. Animals from either group were sacrificed weekly from the start of the treatment along with their respective controls. Progression of hepatic fibrosis, in addition to the effect of vitamin B 12 , was assessed biochemically for liver function biomarkers, liver glycogen, hydroxyproline (HP) and B 12 reserves along with histopathologically by hematoxylin and eosin (H & E) as well immunohistochemical staining for a-SMA expression. Results and discussion: Elevation in the levels of aminotransferases, SALP, total bilirubin and HP was observed in NDMA treated rats, which was concomitant with remarkable depletion in liver glycogen and B 12 reserves (p50.05). Liver biopsies also demonstrated disrupted lobular architecture, collagen amassing and intense fibrosis by NDMA treatment. Immunohistochemical staining showed the presence of activated stellate cells that was dramatically increased up to day 21 in fibrotic rats. Following vitamin B 12 treatment, liver function biomarkers, glycogen contents and hepatic vitamin B 12 reserves were restored in fibrotic rats, significantly. Vitamin B 12 administration also facilitated restoration of normal liver architecture. Conclusion: These findings provide interesting new evidence in favor of protective role for vitamin B 12 against NDMA-induced hepatic fibrosis in rats.

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Section: Discussionsupporting

confidence: 52%

Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Ahmad

Afroz

Gupta

et al. 2014

Pharmaceutical Biology

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“…EGCG has shown the inhibition of activation of IKK·, phosphorylation and subsequent degradation of IκB· (18). In addition, EGCG suppresses the proliferation of hepatic stellate cells and production of extracellular matrix in the hepatic fibrosis (19)(20)(21). Yumei et al reported that EGCG induced the de novo synthesis of glutathione and antifibrogenic effects in passaged rat hepatic stellate cells (22,23).…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate improves nonalcoholic steatohepatitis model mice expressing nuclear sterol regulatory element binding protein-1c in adipose tissue

Ueno

Torimura²,

Nakamura³

et al. 2009

Int J Mol Med

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Abstract. We examined whether or not epigallocatechin-3-gallate (EGCG) improves liver injury of nonalcoholic steatohepatitis (NASH) model mice expressing nuclear sterol regulatory element-binding protein 1c in adipose tissue. nSREBP-1c transgenic C57BL6 mice aged 30 weeks were divided into group 1 (no treatment), group 2 (ascorbic acid alone), group 3 (ascorbic acid and 0.05% EGCG), and group 4 (ascorbic acid and 0.1% EGCG). At 42 weeks, we performed measurement of liver weight to body weight, biochemical assays, morphometry of liver specimens, immunohistochemistry for 8-hydro-2'-deoxyguanosine (8-OhdG), and Western blotting for insulin and TNF-· signalings. Ratio of liver weight to body weight in the high dose EGCG-treated group (group 4) was significantly lower than those of groups 1 and 2 (p<0.05 and <0.01, respectively). Blood ALT, glucose, total cholesterol, and triglyceride levels of group 4 were significantly low compared with those of the EGCGnon-treated group (groups 1 and 2) (p<0.05, respectively). The degrees of steatosis, inflammation, ballooning hepatocytes and Mallory-Denk bodies in group 4 significantly improved compared with those in other groups (p<0.05, respectively). The 8-OhdG immunolocalization in liver tissues of the group 4 obviously decreased compared with those of groups 2 and 3. For Western blotting, the expressions of insulin receptor substrate-1 (IRS-1) and phosphorylated IRS-1 (pIRS-1) in liver tissues of group 4 increased compared with those of groups 2 and 3. On the other hand, the expressions of pAkt, pIKKß and pNF-κB decreased compared with those of groups 2 and 3. From these results, EGCG reduces inflammation, insulin resistance and oxidative stress, and suppresses liver injury in nSREBP-1c transgenic mice. IntroductionAlthough the obesity epidemic is a worldwide phenomenon, the severity of the epidemic differs greatly from region to region. The prevalence of obesity among Japanese adults is 3.4% in males and 3.8% in females, and is around one tenth of that in the USA (1). In addition, currently in Japan almost 30% of adult males and females over 50 years old are obese. This rising incidence of obesity parallels the dramatic increase in fatty liver in these age groups. Based on annual health checks, the prevalence of fatty liver diagnosed by ultrasonography increased from 10% in 1980 to 20-40% in 2000 among adults. Thus, nonalcoholic fatty liver disease (NAFLD) is now emerging as the most common liver disease in Japan (2,3). The recent worldwide rise in the number of patients with nonalcoholic steatohepatitis (NASH) tends to parallel the increase in metabolic syndrome, which includes obesity, type 2 diabetes and hyperlipidemia (4).NAFLD mainly comprises of simple steatosis that is considered benign, however some patients have nonalcoholic steatohepatitis (NASH), which is a clinicopathological entity characterized by the development of hepatic histological changes resembling those induced by excessive alcohol intake that occur in the absence of alcohol abuse (5). Some patients w...

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“…Hydroxysafflor yellow A (HSYA) (for its structure, see Figure 1) is a major constituent in the hydrophilic fraction of Carthamus tinctorius L. (Compositae) (known as Honghua in China), which has been traditionally widely used in traditional Chinese medicine for the treatment of cirrhosis in clinics (Bie et al, 2010). Several lines of evidence indicate that polyphenolic components, including curcumin (Wang et al, 2012), resveratrol (Di Pascoli et al, 2013) and epigallocatechin-3-gallate (Zhen et al, 2007), have antifibrosis activity on liver.…”

Section: Introductionmentioning

confidence: 99%

Alteration of the ERK5 pathway by hydroxysafflor yellow A blocks expression of MEF2C in activated hepatic stellate cellsin vitro: Potential treatment for hepatic fibrogenesis

Dong

Liu

Zou

et al. 2013

Pharmaceutical Biology

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Green tea polyphenol epigallocatechin-3-gallate inhibits oxidative damage and preventive effects on carbon tetrachloride–induced hepatic fibrosis

Cited by 92 publications

References 44 publications

Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Epigallocatechin-3-gallate improves nonalcoholic steatohepatitis model mice expressing nuclear sterol regulatory element binding protein-1c in adipose tissue

Alteration of the ERK5 pathway by hydroxysafflor yellow A blocks expression of MEF2C in activated hepatic stellate cellsin vitro: Potential treatment for hepatic fibrogenesis

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Green tea polyphenol epigallocatechin-3-gallate inhibits oxidative damage and preventive effects on carbon tetrachloride–induced hepatic fibrosis

Cited by 92 publications

References 44 publications

Vitamin B12supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Vitamin B12supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Epigallocatechin-3-gallate improves nonalcoholic steatohepatitis model mice expressing nuclear sterol regulatory element binding protein-1c in adipose tissue

Alteration of the ERK5 pathway by hydroxysafflor yellow A blocks expression of MEF2C in activated hepatic stellate cellsin vitro: Potential treatment for hepatic fibrogenesis

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Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats

Vitamin B₁₂supplement alleviatesN′-nitrosodimethylamine-induced hepatic fibrosis in rats