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Green Tea Extract Protects Against Fibrogenesis Associated With Nonalcoholic Steatohepatitis In Diet‐Induced Obese Rats
Author(s) -
Bower Allyson M,
Park Hea Jin,
Chung Min-Yu,
Lee Jiyoung,
Bruno Richard S
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.363.6
Subject(s) - oxidative stress , hepatic stellate cell , medicine , endocrinology , fibrosis , chemistry , green tea extract , hydroxyproline , liver injury , steatosis , antioxidant , hepatic fibrosis , nonalcoholic fatty liver disease , fatty liver , biochemistry , green tea , food science , disease
Nonalcoholic steatohepatitis (NASH) is characterized by oxidative stress and liver injury that increases fibrosis risk. We hypothesized that the antioxidant activity of green tea extract (GTE) would protect against NASH‐related liver injury, oxidative stress, and fibrosis. Wistar rats (16 wk old, n = 63) were fed a low‐fat (LFD) or high‐fat (HFD) diet containing 0, 1, or 2% GTE for 8 wk. The HFD compared to the LFD increased ( P <0.05) body mass and plasma aspartate (AST) and alanine (ALT) aminotransferases. The HFD also increased hepatic α‐smooth muscle actin (αSMA) expression and hydroxyproline (HYP) concentrations whereas hepatic total glutathione (tGSH) was lower. GTE (1–2%) normalized body mass to that of LFD controls, independent of energy intake. Rats fed GTE had lower ALT and AST compared to those fed a HFD. Rats fed GTE at 2% had lower αSMA whereas both GTE levels normalized HYP. tGSH was greater in rats fed GTE at 2% compared to those fed a HFD. tGSH was inversely related ( P <0.05; r = −0.33 to −0.31) to αSMA and HYP, supporting that oxidative stress induces fibrogenesis. AST was also correlated ( P <0.05; r = 0.30–0.31) to αSMA and HYP, supporting that liver injury promotes fibrogenesis. Thus, GTE protects against fibrogenesis during NASH by reducing hepatic injury and oxidative stress otherwise leading to hepatic stellate cell activation and collagen accumulation. Grant Funding Source : USDA‐NRI