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Green tea extract (GTE) protects against hepatic inflammation by reducing cyclooxygenase‐2 (COX‐2) in a rat model of dietary fat‐induced nonalcoholic steatohepatitis (NASH)
Author(s) -
Chung MinYu,
Noh Sang K,
Masterjohn Chris,
Park Hea Jin,
Clark Richard M,
Park YoungKi,
Lee JiYoung,
Koo Sung I,
Bruno Richard S
Publication year - 2011
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.25.1_supplement.106.2
Subject(s) - medicine , endocrinology , green tea extract , steatosis , chemistry , arachidonic acid , inflammation , malondialdehyde , cyclooxygenase , eicosanoid , phospholipase a2 , nonalcoholic fatty liver disease , oxidative stress , fatty liver , biochemistry , biology , enzyme , food science , disease , green tea
We examined whether GTE protects against inflammation associated with NASH by regulating COX‐2. Wistar rats (16 wk old, n=63) were fed a low‐fat diet (LF) containing no GTE, or a high‐fat diet (HF) containing GTE at 0, 1, or 2% for 8 wk. Rats fed HF developed liver steatosis and had greater ( P <0.05) hepatic malondialdehyde (MDA) and serum alanine aminotransferase (ALT). GTE normalized the levels of hepatic lipid, MDA, and ALT to those of LF controls. The activity and protein expression of hepatic COX‐2 were greater in HF fed controls. GTE normalized COX‐2 activity and decreased its expression below the levels of LF controls. Arachidonic acid (AA) was elevated in the total lipid, phospholipid (PL), and free fatty acid (FFA) fractions of hepatic lipid extract. Although GTE reduced total AA by 6–8% ( P <0.05), the concentrations of AA in the PL and FFA fractions remained unaffected as was cytosolic phospholipase A 2 activity. HF increased cytochrome P 450 2E1 mRNA expression, whereas GTE did not affect its expression. Thus, data suggest that GTE reduces dietary fat‐induced hepatic inflammation and oxidative stress by decreasing the activity and expression of COX‐2, without altering the flux of AA between membrane PL and FFA pools. Additional studies are warranted to define whether GTE suppresses COX‐2 mediated prostaglandin generation. Supported by a USDA‐NRI grant to RSB (2007‐02303). Grant Funding Source: USDA