梓醇调控自噬和凋亡促进H2O2诱导的PC12细胞存活

被引：11

作者：

王园 ^{[1
]}

刘珂 ^{[1
]}

邱邴勋 ^{[1
]}

祝慧凤 ^{[1
]}

王涛 ^{[1
]}

万东 ^{[2
]}

机构：

[1] 西南大学药学院暨中医药学院

[2] 重庆医科大学附属第一医院急诊医学科&重症医学科

来源：

西南大学学报(自然科学版) | 2018年 / 40卷 / 02期

关键词：

梓醇; PC12细胞; 过氧化氢; 凋亡; 自噬;

D O I：

10.13718/j.cnki.xdzk.2018.02.005

中图分类号：

R285 [中药药理学];

学科分类号：

100806 [中药药理学];

摘要：

探讨梓醇对过氧化氢（H2O2）诱导的PC12细胞氧化损伤后调控凋亡和自噬相关分子的机制,采用0.01 mmol,0.1 mmol,1 mmol的梓醇预处理PC12细胞2h后,再用250μmol/L H2O2损伤细胞12h.MTT法检测细胞存活率,设置梓醇低、中、高3个剂量组（0.01 mmol,0.1 mmol,1 mmol）,自噬抑制剂3MA阳性对照组,阴性对照组,H2O2诱导的PC12细胞损伤模型组,采用荧光单标检测LC3Ⅱ的表达,Western blot检测凋亡和自噬相关蛋白Bcl2/Bax,LC3Ⅱ/Ⅰ和Cleaved-caspase 3的表达情况.结果显示,梓醇呈剂量依赖性地提高了H2O2诱导的PC12细胞的存活,并对H2O2诱导的PC12细胞的LC3Ⅱ/Ⅰ,Bcl2/Bax升高蛋白水平表达,降低了Cleaved-caspase 3的表达;随着梓醇浓度的增加,Cleaved-caspase 3的表达减少,而LC3Ⅱ/Ⅰ和Bcl2/Bax的表达在升高.得出梓醇通过恢复凋亡和自噬相关蛋白Bcl2/Bax,LC3Ⅱ/Ⅰ的平衡能够保护PC12细胞免于H2O2诱导的氧化损伤.

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页码：27 / 34

页数：8

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