大黄素上调Sirt2减轻脂多糖致RAW264.7细胞的氧化应激反应

Emodin upregulates the Sirt2 to attenuate LPS-induced oxidative stress response in RAW264.7 cells

目的探究大黄素(Emodin)对脂多糖(LPS)刺激的小鼠巨噬细胞系(RAW264.7)氧化应激反应的影响及其机制。方法利用LPS、RAW264.7细胞和大黄素进行研究。设空白对照(Control)组、LPS(1μg/mL)组、LPS(1μg/mL)+大黄素(15μmol/L预处理)组,在予LPS处理后6、12、18 h检测丙二醛(MDA)含量、细胞内活性氧(ROS)水平以及沉默信息调节因子2(Sirt2)表达水平等。使用Sirt2抑制剂AGK2(20μmol/L)预处理RAW264.7细胞,仅在予LPS处理后6 h检测上述指标。结果与Control组相比,各时间点LPS组RAW264.7细胞的MDA含量、ROS水平及Sirt2 mRNA水平及蛋白表达水平均增加(P<0.05)。LPS+大黄素组与LPS组相比,各时间点的RAW264.7细胞Sirt2 mRNA水平及蛋白水平均显著升高(P<0.05),ROS水平均降低(P<0.05);6、18 h的MDA含量均降低(P<0.05)。与LPS+大黄素组相比,LPS+大黄素+AGK2组Sirt2 mRNA及蛋白表达水平均降低,且MDA含量、ROS水平均增加(P<0.05)。结论LPS刺激RAW264.7细胞后氧化应激反应显著增加,大黄素可通过Sirt2在LPS刺激RAW264.7细胞模型中抑制氧化应激反应。

Objective The aim of this study was to investigate the impact and mechanisms of emodin on oxidative stress response in lipopolysaccharide(LPS)-induced murine mononuclear macrophages(RAW264.7).Methods Involved the use of LPS,RAW264.7 cells,and emodin.Experimental groups included a control group,LPS(1μg/mL)group,and LPS(1μg/mL)+emodin(15μmmol/L)pretreatment group.Aldehyde malondialdehyde(MDA)content,intracellular reactive oxygen species(ROS)levels,and silent information regulator 2(Sirt2)expression were evaluated at 6,12,and 18 hours after LPS exposure.Additionally,RAW264.7 cells were pretreated with Sirt2 inhibitor AGK2(20μmol/L)followed by LPS stimulation,and the above-mentioned parameters were assessed at 6 hours.Results Compared to the control group,MDA content,ROS levels,Sirt2 mRNA,and protein expression in RAW264.7 cells in the LPS group increased at all time points(all P<0.05).At 6 and 18 hours,MDA content and ROS levels in RAW264.7 cells in the LPS+emodin group decreased significantly(all P<0.05),while at 12 hours,ROS levels were lower in the LPS group compared to the LPS+emodin group(P<0.05).Sirt2 mRNA and protein levels significantly increased at all time points(all P<0.05)compared to the LPS group.In the LPS+emodin+AGK2 group,Sirt2 mRNA and protein levels decreased,and MDA content and ROS levels increased compared to the LPS+emodin group(all P<0.05).Conclusion LPS-induced oxidative stress in RAW264.7 cells and emodin attenuate LPS-induced oxidative stress in RAW264.7 cells through Sirt2.