Protective effect of L-theanine on carbon tetrachloride-induced acute liver injury in mice
Protective effect of L-theanine on carbon tetrachloride-induced acute liver injury in mice
复制标题
L-茶氨酸对四氯化碳所致小鼠急性肝损伤的保护作用
DOI：
10.1016/j.bbrc.2012.05.022
复制
发表时间：
2012-06-01
影响因子：
3.1
通讯作者：
Luo, Lan
中科院分区：
文献类型：
--
作者：
Jiang, Wei;Gao, Min;Luo, Lan
研究了茶叶中特有的氨基酸L-茶氨酸对四氯化碳（CCl 4）诱导的小鼠肝损伤的影响。在注射CCl 4（10 ml/kg的0.2% CCl 4橄榄油溶液）之前，小鼠每天一次经口给予L-茶氨酸（50、100或200 mg/kg）预处理7天。L-茶氨酸剂量依赖性地抑制CCl_4引起的小鼠血清ALT、AST活性和胆红素水平的升高及肝组织病理学改变。L-茶氨酸能显著抑制CCl 4诱导的脂质过氧化反应，降低肝脏GSH含量和抗氧化酶活性。进一步研究表明，L-茶氨酸通过下调细胞色素P450 2 E1（CYP 2 E1）抑制四氯化碳代谢活化。因此，L-茶氨酸抑制氧化应激介导的炎症反应，包括血清中TNF-α和IL-1 β的增加，以及肝脏中环氧合酶-2（考克斯-2）和诱导型一氧化氮合酶（iNOS）的表达。CCl 4诱导的凋亡相关蛋白的激活，包括caspase-3和PARP在小鼠肝脏中也阻止了L-茶氨酸治疗。综上所述，L-茶氨酸通过抑制CCl 4的代谢活化和防止CCl 4诱导的小鼠肝脏抗氧化能力降低来减轻炎症反应和肝细胞凋亡，从而保护小鼠免受CCl 4诱导的急性肝损伤。(C)2012 Elsevier Inc. All rights reserved.
We studied effects of L-theanine, a unique amino acid in tea, on carbon tetrachloride (CCl4)-induced liver injury in mice. The mice were pre-treated orally with L-theanine (50, 100 or 200 mg/kg) once daily for seven days before CCl4 (10 ml/kg of 0.2% CCl4 solution in olive oil) injection. L-theanine dose-dependently suppressed the increase of serum activity of ALT and AST and bilirubin level as well as liver histopathological changes induced by CCl4 in mice. L-theanine significantly prevented CCl4-induced production of lipid peroxidation and decrease of hepatic GSH content and antioxidant enzymes activities. Our further studies demonstrated that L-theanine inhibited metabolic activation of CCl4 through down-regulating cytochrome P450 2E1 (CYP2E1). As a consequence, L-theanine inhibited oxidative stress-mediated inflammatory response which included the increase of TNF-alpha and IL-1 beta in sera, and expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in livers. CCl4-induced activation of apoptotic related proteins including caspase-3 and PARP in mouse livers was also prevented by L-theanine treatment. In summary, L-theanine protects mice against CCl4-induced acute liver injury through inhibiting metabolic activation of CCl4 and preventing CCl4-induced reduction of anti-oxidant capacity in mouse livers to relieve inflammatory response and hepatocyte apoptosis. (C) 2012 Elsevier Inc. All rights reserved.