title: Green Tea Lowers Hepatic COX-2 and Prostaglandin E2 in Rats with Dietary Fat-Induced Nonalcoholic Steatohepatitis.
abstract: Green tea extract (GTE) protects against nonalcoholic steatohepatitis (NASH) by decreasing hepatic steatosis and nuclear factor kappa B (NFκB) activation. We hypothesized that hypolipidemic and anti-inflammatory activities of GTE would protect against NASH by reducing cyclooxygenase-2 (COX-2), an NFκB-dependent enzyme, and prostaglandin E2 (PGE2) in a dietary fat-induced obese model. Male Wistar rats were fed a low-fat diet containing no GTE or a high-fat (HF) diet containing GTE at 0%, 1%, or 2% for 8 weeks. Insulin resistance and total hepatic fatty acids increased following HF feeding (P<.05) and these were normalized by GTE at 1-2%. GTE (1-2%) normalized hepatic malondialdehyde without affecting cytochrome P450 2E1 mRNA expression, which was otherwise increased by HF feeding. HF-mediated increases in hepatic COX-2 protein and activity as well as PGE2 concentrations were normalized by GTE (1-2%). COX-2 activity and PGE2 were correlated to each other, and to serum alanine aminotransferase (ALT) and hepatic NFκB-binding activity (P<.05; r=0.28-0.49). GTE attenuated HF-mediated increases in total hepatic n-6 and n-3, without affecting the n-6/n-3 ratio. GTE did not affect HF-mediated increases in n-6 in nonesterified fatty acid (NEFA) and phospholipid pools, whereas n-3 and n-6/n-3 in both pools were unaffected by GTE and HF feeding. GTE decreased total hepatic arachidonic acid without affecting HF-mediated increases in arachidonic acid in NEFA or phospholipid pools. Thus, GTE attenuates lipid peroxidation and PGE2 accumulation by decreasing COX-2 activity independent of arachidonic acid availability and supports an additional mechanism by which GTE protects against liver injury during NASH in an HF-feeding model.
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.|2Division of Metabolism and Functionality Research, Korea Food Research Institute, Seongnam, South Korea.
authors.forename: Min-Yu
authors.initials: MY
authors.lastname: Chung
authors.affiliation: 3Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA.
authors.forename: Eunice
authors.initials: E
authors.lastname: Mah
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
authors.forename: Christopher
authors.initials: C
authors.lastname: Masterjohn
authors.affiliation: 4Department of Food and Nutrition, Changwon National University, Changwon, South Korea.
authors.forename: Sang K
authors.initials: SK
authors.lastname: Noh
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.|5Department of Foods and Nutrition, University of Georgia, Athens, Georgia, USA.
authors.forename: Hea Jin
authors.initials: HJ
authors.lastname: Park
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
authors.forename: Richard M
authors.initials: RM
authors.lastname: Clark
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
authors.forename: Young-Ki
authors.initials: YK
authors.lastname: Park
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
authors.forename: Ji-Young
authors.initials: JY
authors.lastname: Lee
authors.affiliation: 1Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.|3Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA.
authors.forename: Richard S
authors.initials: RS
authors.lastname: Bruno
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D028241:Camellia sinensis; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D059305:Diet, High-Fat; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D007333:Insulin Resistance; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D017208:Rats, Wistar; D013662:Tea
chemical_list: D000893:Anti-Inflammatory Agents; D004041:Dietary Fats; D005227:Fatty Acids; D000960:Hypolipidemic Agents; D016328:NF-kappa B; D010936:Plant Extracts; D013662:Tea; D008315:Malondialdehyde; D051546:Cyclooxygenase 2; D000410:Alanine Transaminase; D015232:Dinoprostone
keywords: cyclooxygenase; green tea; high-fat feeding; nonalcoholic steatohepatitis; nuclear factor kappa B; prostaglandin