Zou Weiying, Liu Wenwen, Yang Bei, Wu Lei, Yang Jianhua, Zou Ting, Liu Fangming, Xia Liping, Zhang Dalei
Department of Physiology, Medical College of Nanchang University, Nanchang 330006, PR China.
Library, Nanchang University, Nanchang 330006, PR China.
Int Immunopharmacol. 2015 Sep;28(1):129-35. doi: 10.1016/j.intimp.2015.05.043. Epub 2015 Jun 6.
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.
本研究的目的是探讨槲皮素（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。将小鼠连续14天单独灌胃给予PFOA（10mg/kg/天）或与Que（75mg/kg/天）联合灌胃。通过测量形态学变化、肝功能、氧化应激、炎症反应和肝细胞凋亡来评估肝损伤。与单独用PFOA处理的小鼠相比，同时补充Que可显著降低肝损伤指标丙氨酸转氨酶、天冬氨酸转氨酶、碱性磷酸酶、乳酸脱氢酶和总胆汁酸的血清水平。此外，Que处理抑制了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，降低了促炎细胞因子白细胞介素6、环氧化酶-2和C反应蛋白的水平，并减少了PFOA处理小鼠肝脏中TUNEL阳性细胞的数量。这些结果与肝脏组织病理学相结合表明，Que通过减轻氧化应激、缓解炎症和抑制肝细胞凋亡等机制对PFOA诱导的肝损伤具有潜在的保护作用。
