目的:探究姜黄素(Cur)对H2O2诱导的大鼠施万细胞来源细胞系RSC96细胞焦亡的抑制作用及其机制.方法:选取大鼠施万细胞来源细胞系RSC96细胞,给予H2O2预处理,建立周围神经氧化损伤模型,同时给予Cur干预.CCK-8法检测细胞活力,乳酸脱氢酶(LDH)试剂盒检测细胞LDH漏出率,酶联免疫吸附试验(ELISA)检测细胞 IL-1β 分泌水平,Western Blot 检测 NLRP3、caspase-1、cleaved caspase-1、GSDMD、GSDMD-N 及IL-1β蛋白表达水平.结果:姜黄素可显著提高H2O2处理的RSC96细胞活力,降低LDH漏出率,下调IL-1β分泌水平,同时抑制NLRP3、caspase-1、cleaved caspase-1、GSDMD、GSDMD-N及IL-1β的蛋白表达.结论:姜黄素可通过NLRP3/caspase-1/GSDMD信号通路抑制H2O2诱导的RSC96细胞焦亡,从而发挥神经保护作用.
Abstract
Objective:To investigate the inhibitory effect and mechanism of curcumin on the rat Schwann cell derived cell line RSC96 cells pyroptosis induced by hydrogen peroxide.Methods:The rat Schwann cell derived cell line RSC96 cells were selected and treated with hydrogen peroxide to establish the peripheral nerve oxidative injury mod-el,curcumin intervention was also given.Cell viability was detected by CCK-8 kit.Lactate dehydrogenase(LDH)kit was used to detect the LDH leakage rate.The level of IL-1 β was detected by enzyme linked immunosorbent assay(ELISA).The protein expression levels of NLRP3,caspase-1,cleaved caspase-1,GSDMD,GSDMD-N and IL-1 βwere detected by Western Blot.Results:Cur significantly increased the viability of RSC96 cells treated with H2O2,decreased LDH leakage rate,down-regulated IL-1 β secretion,and inhibited the protein expression of NLRP3,caspase-1,cleaved caspase-1,GSDMD,GSDMD-N,and IL-1 β.Conclusion:Curcumin can inhibit hydrogen peroxide-induced pyroptosis of RSC96 cells through the NLRP3/caspase-1/GSDMD signaling pathway,thus exerting neuroprotective effect.
维普
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