Quercetin protects against perfluorooctanoic acid-induced liver injury by attenuating oxidative stress and inflammatory response in mice.

Quercetin protects against perfluorooctanoic acid-induced liver injury by attenuating oxidative stress and inflammatory response in mice.
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DOI:
10.1016/j.intimp.2015.05.043
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发表时间:
2015-09
影响因子:
5.6
通讯作者:
Weiying Zou;Wenwen Liu;Bei Yang;Lei Wu;Jianhua Yang;T. Zou;Fangming Liu;Liping Xia;Dalei Z
Weiying Zou;Wenwen Liu;Bei Yang;Lei Wu;Jianhua Yang;T. Zou;Fangming Liu;Liping Xia;Dalei Z
中科院分区:
医学2区
文献类型:
--
作者:
Weiying Zou;Wenwen Liu;Bei Yang;Lei Wu;Jianhua Yang;T. Zou;Fangming Liu;Liping Xia;Dalei Z

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研究槲皮素(Que)对全氟辛酸(PFOA)诱导的小鼠肝损伤的保护作用及其可能的作用机制。小鼠连续14天单独或与Que(75 mg/kg/天)联合灌胃给予PFOA(10 mg/kg/天)。通过检测肝组织形态学、肝功能、氧化应激、炎症反应和肝细胞凋亡来评价肝损伤。与仅用PFOA处理的小鼠相比,同时补充Que显著降低肝损伤指标丙氨酸氨基转移酶、天冬氨酸氨基转移酶、碱性磷酸酶、乳酸脱氢酶和总胆汁酸的血清水平。此外,Que处理抑制氧化应激生物标志物丙二醛、过氧化氢和8-羟基-2 ′-脱氧鸟苷的产生,降低促炎细胞因子白细胞介素6、环氧合酶-2和C-反应蛋白的水平,并减少PFOA处理小鼠肝脏中TUNEL阳性细胞的数量。这些结果结合肝组织病理学表明,Que通过涉及减轻氧化应激,减轻炎症和抑制肝细胞凋亡的机制对PFOA诱导的肝损伤表现出潜在的保护作用。
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 (10 mg/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.