文献类型：期刊文献

中文题名：壳寡糖减轻过氧化氢诱导的SK-N-SH细胞氧化损伤机制研究

英文题名：Mechanism of chitosan oligosaccharides attenuated oxidative damage induced by H_(2)O_(2) in SK-N-SH cells

作者：张晓霞[1];李筱筱[1];孙雅煊[1];戴雪伶[1]

第一作者：张晓霞

机构：[1]北京联合大学生物化学工程学院,生物活性物质与功能食品北京市重点实验室,北京100191

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

年份：2021

卷号：47

期号：14

起止页码：57-62

中文期刊名：食品与发酵工业

外文期刊名：Food and Fermentation Industries

收录：CSTPCD;;北大核心:【北大核心2020】；CSCD:【CSCD2021_2022】；

基金：北京市自然科学基金(6164030);北京市优秀人才资助项目(2015000020124G049);北京市生物活性物质和功能性食品重点实验室开放课题;北京联合大学科研资助项目(XP202007);北京联合大学研究生资助项目。

语种：中文

中文关键词：壳寡糖;H2 O2;细胞凋亡;Bcl-2;Bax;Nrf2;HO-1

外文关键词：chitosan oligosaccharides;H2 O2;cell apoptosis;Bcl-2;Bax;Nrf2;HO-1

摘要：为探讨壳寡糖(chitosan oligosaccharide,COS)对H_(2)O_(2)诱导的人神经母细胞瘤SK-N-SH细胞损伤的保护作用及其机制,利用H_(2)O_(2)建立体外氧化损伤模型,MTT法检测细胞存活率,酶活性检测乳酸脱氢酶(lactate dehydrogenase,LDH)的释放情况,JC-10检测细胞线粒体膜电位的变化,ATP发光测定试剂盒检测细胞内ATP水平,蛋白质免疫印迹(Western Blot)检测细胞中Bcl-2、Bax、Nrf2和HO-1蛋白的表达。结果表明,与H_(2)O_(2)组相比,COS预处理可有效提高H_(2)O_(2)诱导的细胞存活率,有效抑制细胞内LDH的释放,明显恢复线粒体膜电位,提高细胞内ATP水平,促进Bcl-2、Nrf2和HO-1蛋白的表达,抑制Bax蛋白的表达。COS可保护SK-N-SH细胞免受H_(2)O_(2)诱导的氧化损伤,抑制细胞凋亡并促进抗氧化蛋白表达水平。
To investigate the protective effect of chitosan oligosaccharides(COS)on the cellular damage of SK-N-SH cells induced by H_(2)O_(2),H_(2)O_(2) was used to establish an in vitro oxidative damage model.The cell viability was detected by MTT,and the release of lactate dehydrogenase(LDH)was detected by kit.JC-10 was used to detect changes in cell mitochondrial membrane potential,ATP luminescence assay kit was used to detect intracellular ATP level,and the expression of Bcl-2,Bax,Nrf2 and HO-1 protein was detected by Western Blot.Results showed that compared with the H_(2)O_(2) group,COS pretreatment could effectively increase the cell survival rate induced by H_(2)O_(2),markedly inhibit the release of intracellular LDH,significantly restore mitochondrial membrane potential,increase intracellular ATP levels,and promote the expression of Bcl-2,Nrf2 and HO-1 protein,inhibit the expression of Bax protein.COS could protect SK-N-SH cells from oxidative damage induced by H_(2)O_(2) via inhibiting cell apoptosis and promoting the expression of antioxidant proteins.