title: Emblica officinalis Gaertn. attentuates N-nitrosodiethylamine-induced apoptosis, autophagy, and inflammation in rat livers.
abstract: Inflammation and oxidative stress contribute to liver injury. Amla (Emblica officinalis Gaertn.) is rich in vitamin C, gallic acid, flavonoids, and tannins, which may protect against hepatoxicity-induced liver injury. We elucidated the effects of supplementary Amla (100 mg/kg of body weight) on N-nitrosodiethylamine-induced injury by evaluating reactive oxygen species (ROS) responses in the liver and bile, the degree of accumulated leukocytes and Kupffer cell infiltration, 3-nitrotyrosine and 4-hydroxynonenal stains, apoptosis and autophagy, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (γ-GT) levels, and antioxidant/oxidant enzymes in rats. Amla was more potent than vitamin C in scavenging O₂⁻·, hydrogen peroxide, and nitric oxide. N-Nitrosodiethylamine increased ROS production in liver and bile, hepatic Kupffer cell and leukocyte infiltration, 3-nitrotyrosine and 4-hydroxynonenal accumulations, apoptosis and autophagy, and plasma ALT, AST, and γ-GT levels in the rats, decreased hepatic manganese superoxide dismutase (MnSOD) and catalase protein expressions, and enhanced inducible nitric oxide synthase (iNOS) and cytochrome P450 2E1 (CYP2E1) protein expressions. Amla significantly preserved MnSOD and catalase expressions and decreased iNOS and CYP2E1 protein expressions in N-nitrosodiethylamine-treated livers. Amla decreased N-nitrosodiethylamine-enhanced hepatic apoptosis and autophagy appearances via down-regulation of the Bax/Bcl-2 ratio and Beclin-1 expression. Thus Amla supplementation counteracts N-nitrosodiethylamine-induced liver injury via its antioxidant, anti-inflammation, anti-apoptosis, and anti-autophagy properties.
authors.affiliation: Division of General Surgery, Far-Eastern Memorial Hospital, Taipei, Taiwan.
authors.forename: Kuo-Hsin
authors.initials: KH
authors.lastname: Chen
authors.forename: Bor-Ru
authors.initials: BR
authors.lastname: Lin
authors.forename: Chiang-Ting
authors.initials: CT
authors.lastname: Chien
authors.forename: Chien-Hsin
authors.initials: CH
authors.lastname: Ho
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D001343:Autophagy / Q000187:drug effects*; D004052:Diethylnitrosamine / Q000633:toxicity*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000276:immunology* / Q000503:physiopathology; D008113:Liver Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D029842:Phyllanthus emblica / Q000737:chemistry*; D010936:Plant Extracts / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D005723:gamma-Glutamyltransferase / Q000378:metabolism; D000099156:Superoxide Dismutase 2
chemical_list: D000975:Antioxidants; D004052:Diethylnitrosamine; D052247:Nitric Oxide Synthase Type II; D010936:Plant Extracts; D013482:Superoxide Dismutase; D005723:gamma-Glutamyltransferase; D000099156:Superoxide Dismutase 2