玉米黄素对内质网应激引发的SH-SY5Y细胞凋亡的保护作用  

Protection of Zeaxanthin on Endoplasmic Reticulum Stress-Induced Apoptosisin SH-SY5Y Cells

作　　者：商迎辉[1] 魏俊 李梦洁 刘芸如 黄汉昌[1] 劳凤学[1] Shang Yinghui;Wei Jun;Li Mengjie;Liu Yunru;Huang Hanchang;Lao Fengxue(Beijing Key Laboratory of Bioactive Substances and Functional Foods,Institute of Functional Factors and Brain Science,Beijing Union University,Beijing 100191)

机构地区：[1]北京市生物活性物质和功能食品重点实验室、北京联合大学功能因子与脑科学研究院,北京100191

出　　处：《中国食品学报》2023年第7期37-44,共8页Journal of Chinese Institute Of Food Science and Technology

基　　金：国家自然科学基金面上项目(31471587)。

摘　　要：目的:研究玉米黄素对内质网应激引起的细胞凋亡的保护作用。试验分为空白对照组、衣霉素(TM)损伤组(5μg/mL)、玉米黄素保护组(5μmol/L)和损伤加保护组。采用Caspase 3试剂盒检测Caspase 3活性的变化;采用Western Blot法测定凋亡相关蛋白PERK、CHOP,PERK下游信号分子elF2α和ATF4,以及自噬相关蛋白Beclin 1。结果显示:与TM模型组相比,玉米黄素处理后PERK及其下游调控蛋白elF2α和ATF4的表达能力显著下降(P<0.01),Beclin 1的水平显著升高(P<0.01)。与未加自噬抑制剂相比,玉米黄素组的GRP78水平显著升高(P<0.01)。与对照组相比,TM模型组的CHOP蛋白的表达水平极显著升高(P<0.01),而玉米黄素处理组CHOP蛋白的表达水平极显著低于TM模型组(P<0.01)。结论:玉米黄素能减轻由内质网应激引起的损伤作用,并且可逆转TM引起的损伤。其作用机制是:玉米黄素通过抑制PERK通路,进而抑制GRP78与ERS感受器的分离,降低促凋亡因子CHOP的水平,通过调控保护性自噬来缓解ERS。Objective:To study the protective effect of zeaxanthin on endoplasmic reticulum stress-induced apoptosis.The research was divided into blank control group,TM injury group(5μg/mL),zeaxanthin protection group(5μmol/L)and injury plus protection group.The Caspase 3 activity detection kit is used for detecting changes of Caspase 3 enzyme activity.The apoptosis-related proteins PERK and CHOP,the downstream signal molecules elF2αand ATF4 of PERK,and the autophagy-related protein Beclin 1 were determined by Western Blot.The results showed that compared with the TM model group,the expressions of PERK and its downstream regulatory proteins elF2αand ATF4 after zeaxanthin treatment were significantly decreased(P<0.01),and the level of Beclin 1 was significantly increased(P<0.01).The level of GRP78 in the zeaxanthin group was significantly higher than that in the absence of 3MA autophagy inhibitor(P<0.01).Compared with the control group,the CHOP protein expression level in the TM model group was significantly increased(P<0.01),while the CHOP protein expression level in the zeaxanthin treatment group was significantly lower than that in the TM model group(P<0.01).Conclusion:Zeaxanthin can reduce the damage caused by endoplasmic reticulum stress and reverse the damage caused by TM to a certain extent.The mechanism is that by inhibiting the PERK pathway and further inhibiting the separation of GRP78 and ERS receptors,the level of pro-apoptotic factor CHOP is reduced,and alleviate ERS by regulating protective autophagy.

关 键 词：玉米黄素 内质网应激 SH-SY5Y细胞 细胞凋亡 

分 类 号：TS201.4[轻工技术与工程—食品科学]