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余甘子减轻 N-亚硝基二乙胺诱导的大鼠肝脏细胞凋亡、自噬和炎症。

Emblica officinalis Gaertn. attentuates N-nitrosodiethylamine-induced apoptosis, autophagy, and inflammation in rat livers.

机构信息

Division of General Surgery, Far-Eastern Memorial Hospital, Taipei, Taiwan.

出版信息

J Med Food. 2011 Jul-Aug;14(7-8):746-55. doi: 10.1089/jmf.2010.1459.

DOI:10.1089/jmf.2010.1459
PMID:21761987
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.

摘要

炎症和氧化应激导致肝损伤。余甘子(Emblica officinalis Gaertn.)富含维生素 C、没食子酸、类黄酮和单宁酸,可预防肝毒性引起的肝损伤。我们通过评估肝脏和胆汁中的活性氧(ROS)反应、白细胞和枯否细胞积累的程度、3-硝基酪氨酸和 4-羟基壬烯醛染色、凋亡和自噬、血浆天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和γ-谷氨酰转肽酶(γ-GT)水平以及抗氧化/氧化酶,阐明了补充余甘子(100mg/kg 体重)对 N-亚硝基二乙胺诱导的损伤的作用。余甘子比维生素 C 更能清除 O₂⁻·、过氧化氢和一氧化氮。N-亚硝基二乙胺增加了肝脏和胆汁中 ROS 的产生、肝枯否细胞和白细胞浸润、3-硝基酪氨酸和 4-羟基壬烯醛的积累、凋亡和自噬以及血浆 ALT、AST 和 γ-GT 水平在大鼠中,降低了肝锰超氧化物歧化酶(MnSOD)和过氧化氢酶蛋白表达,并增强了诱导型一氧化氮合酶(iNOS)和细胞色素 P450 2E1(CYP2E1)蛋白表达。余甘子在 N-亚硝基二乙胺处理的肝脏中显著保存了 MnSOD 和过氧化氢酶的表达,并降低了 iNOS 和 CYP2E1 蛋白的表达。余甘子通过下调 Bax/Bcl-2 比值和 Beclin-1 表达,减少了 N-亚硝基二乙胺增强的肝凋亡和自噬表现。因此,余甘子补充剂通过其抗氧化、抗炎、抗凋亡和抗自噬特性来抵抗 N-亚硝基二乙胺引起的肝损伤。

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