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Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-κB Pathway

机译:槲皮素预处理通过抑制ERK / NF-κB途径抑制肝缺血再灌注诱导的细胞凋亡和自噬

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Background. Hepatic ischemia reperfusion (IR) injury is a common phenomenon in transplantation or trauma. The aim of the present study was to determine the protective effect of quercetin (QE) on hepatic IR injury via the ERK/NF-κB pathway. Methods. Mice were randomized into the sham, IR, QE100?+?IR, and QE200?+?IR groups. Quercetin was administered intragastrically daily at two doses (100?mg/kg and 200?mg/kg) for 5 days prior to IR injury. The expression levels of liver enzymes, inflammatory cytokines, and other marker proteins were determined at 2, 8, and 24 hours after IR. And they were compared among these groups. Results. Compared with the IR group, the treatment of QE reduced the release of cytokines, leading to inhibition of apoptosis and autophagy via downregulation of the ERK/NF-κB pathway in this model of hepatic IR injury. Conclusion. Apoptosis and autophagy caused by hepatic IR injury were inhibited by QE following a reduction in the release of inflammatory cytokines, and the relationship between the two may be associated with inactivation of the ERK/NF-κB pathway.
机译:背景。肝脏缺血再灌注(IR)损伤是移植或创伤中的常见现象。本研究的目的是通过ERK / NF-κB途径确定槲皮素(QE)对肝脏红外损伤的保护作用。方法。将小鼠随机分成假,IR,QE100?+ΔIR和QE200?+?IR组。在IR损伤之前,每次用两种剂量(100×mg / kg和200×mg / kg),槲皮素每天服用胃内每天施用5天。在IR后2,8和24小时测定肝酶,炎症细胞因子和其他标记蛋白的表达水平。他们在这些群体中进行了比较。结果。与IR组相比,QE的治疗减少了细胞因子的释放,导致通过在该肝脏IR损伤模型中的ERK / NF-κB途径下调凋亡和自噬抑制。结论。在炎症细胞因子的释放减少后,QE抑制了由肝红外损伤引起的凋亡和自噬,并且两者之间的关系可能与ERK / NF-κB途径的失活相关。

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