氧化应激
乳酸脱氢酶
促炎细胞因子
化学
丙二醛
肝损伤
碱性磷酸酶
药理学
内分泌学
内科学
细胞凋亡
肝功能
丙氨酸转氨酶
炎症
生物化学
医学
酶
作者
Weiying Zou,Wenwen Liu,Bei Yang,Lei Wu,Jianhua Yang,Ting Zou,Fangming Liu,Liping Xia,Dalei Zhang
标识
DOI:10.1016/j.intimp.2015.05.043
摘要
The aim of the present study was to investigate the protective effect of quercetin (Que) against perfluorooctanoic acid (PFOA)-induced liver injury in mice and its possible mechanisms of action. Mice were intragastrically administered PFOA (10mg/kg/day) alone or in combination with Que (75 mg/kg/day) for 14 consecutive days. The hepatic injury was evaluated by measuring morphological changes, liver function, oxidative stress, inflammatory response and hepatocellular apoptosis. Compared with mice treated with PFOA alone, simultaneous supplementation of Que significantly decreased serum levels of liver injury indicators alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase and total bile acids. Moreover, Que treatment inhibited the production of oxidative stress biomarkers malondialdehyde, hydrogen peroxide and 8-hydroxy-2'-deoxyguanosine, reduced the levels of proinflammatory cytokines interleukin 6, cyclooxygenase-2 and C-reactive protein, and decreased the number of TUNEL-positive cells in the liver of PFOA-treated mice. These results combined with liver histopathology demonstrated that Que exhibited a potential protective effect against PFOA-induced liver damage via mechanisms involving the attenuation of oxidative stress, alleviation of inflammation and inhibition of hepatocellular apoptosis.
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