罗汉果皂苷Ⅴ通过PI3K/Akt通路抑制过氧化氢诱导的MIN6细胞氧化损伤  

MogrosideⅤinhibits H_(2)O_(2)-induced oxidative damage in MIN6 cells by PI3K/Akt pathway

作　　者：韩梦洁 王娟[1] 刘国翔 李婷 周璐炜 陈旭[1] HAN Meng-jie;WANG Juan;LIU Guo-xiang;LI Ting;ZHOU Lu-wei;CHEN Xu(Guilin Medical University,Guilin,Guangxi 541100,China)

机构地区：[1]桂林医学院药学院,广西桂林541100

出　　处：《中国药理学通报》2022年第9期1363-1368,共6页Chinese Pharmacological Bulletin

基　　金：广西省第四批创新驱动发展专项资金项目(桂科AA19254025);国家自然科学基金资助项目(No 81760663);第四批八桂学者2017年专项经费(No[2017]143号)。

摘　　要：目的探讨罗汉果皂苷Ⅴ(mogroside V,MV)对过氧化氢(hydrogen peroxide,H_(2)O_(2))诱导的小鼠胰岛β细胞株MIN6细胞氧化损伤的保护作用,其机制是否与PI3K/Akt信号通路有关。方法MV预处理后,用500μmol·L^(-1)H_(2)O_(2)处理MIN6细胞,MTT法检测MIN6细胞活力。流式细胞术检测各组活性氧(reactive oxygen species,ROS)水平及细胞凋亡率。Western blot检测凋亡相关蛋白Bcl-2、PCNA以及PI3K/Akt信号通路中Akt和p-Akt蛋白表达情况。结果H_(2)O_(2)能够明显抑制MIN6细胞增殖,诱导ROS产生和细胞凋亡,降低Bcl-2、PCNA、Akt和p-Akt的表达。MV预处理后,Bcl-2、PCNA以及Akt和p-Akt的表达增加,MIN6细胞活力增加。此外,MV可部分逆转Akt抑制剂MK2206(5μmol·L^(-1))对MIN6细胞的凋亡和氧化应激作用。结论MV对H_(2)O_(2)诱导的MIN6细胞氧化损伤具有保护作用,其机制是通过激活PI3K/Akt信号通路来实现的。Aim To investigate the protective effect of mogrosideⅤon hydrogen peroxide(H_(2)O_(2))-induced oxidative stress response in mouse isletβcells MIN6 and the relation of its mechanism to PI3K/Akt signaling pathway.Methods MIN6 cells were treated with 500μmol·L^(-1)H_(2)O_(2) after mogroside V,and cell viability was detected by MTT.The release of reactive oxygen species(ROS)and apoptotic percentage of MIN6 cells were determined by flow cytometry.The expressions of apoptosis-related factor Bcl-2,proliferation-related factor PCNA,protein Akt and p-Akt were determined by Western blot.Results H_(2)O_(2) restrained the proliferation of MIN6 cells obviously,induced ROS production and apoptosis,and reduced the expression of Bcl-2 and PCNA.The expressions of protein Akt and p-Akt decreased.After treatment of mogrosideⅤ,the release of ROS decreased,and the apoptosis of MIN6 cells was inhibited.The expression levels of apoptosis-related protein Bcl-2 and proliferation-related protein PCNA were reversed.The expressions of protein Akt and P-Akt increased.The viability of MIN6 cells induced by H_(2)O_(2) increased.In addition,mogrosideⅤpartly reversed the apoptosis induction and ROS production of Akt inhibitor MK2206(5μmol·L^(-1))on MIN6 cells.Conclusions MogrosideⅤhas protective effect on H_(2)O_(2)-induced oxidative damage in MIN6 cells and its mechanism is related to PI3K/Akt signaling pathway.

关 键 词：罗汉果皂苷Ⅴ 过氧化氢 PI3K/AKT MK2206 氧化损伤 胰岛MIN6细胞 

分 类 号：R-332[医药卫生] R284.1R322.57R329.25R349.1