摘要
[目的]探讨牛蒡苷(ARC)对皮质酮(CORT)诱导大鼠嗜铬细胞瘤细胞系(PC12)细胞损伤的保护作用及其机制.[方法]将PC12细胞分为正常组(未给予任何处理)、模型组(CORT处理未给药)、ARC低剂量组(CORT+50μmol/L ARC)及ARC高剂量组(CORT+100μmol/L ARC).采用MTS法检测细胞存活率,LDH法检测LDH释放率,Annexin V染色法检测细胞凋亡率,蛋白免疫印迹法检测凋亡蛋白B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2相关X蛋白(Bax)、天冬氨酸蛋白水解酶3(Caspase-3)及高迁移率族蛋白1(HMGB1)蛋白的表达情况.[结果]与正常组比较,模型组细胞存活率显著降低(P<0.001),LDH释放率、细胞凋亡率均显著升高(P<0.001),Bcl-2蛋白表达水平显著降低(P<0.001),Bax、Caspase-3及HMGB1蛋白表达水平显著升高(P<0.001).与模型组比较,给予不同浓度的ARC(100、50μmol/L)组细胞存活率均显著升高(P<0.001,P<0.01),LDH释放率、细胞凋亡率及坏死率均显著降低(P<0.001,P<0.01),Bcl-2蛋白表达水平显著升高(P<0.001,P<0.05),Bax、Caspase-3及HMGB1蛋白表达水平均显著降低(P<0.001,P<0.01).[结论]ARC对CORT诱导的PC12细胞损伤具有保护作用,其机制可能与调节凋亡通路抑制凋亡和抑制HMGB1向细胞质转移有关系.
OBJECTIVE To investigate the protective effect of arctiin(ARC)on rat pheochromocytoma cell line(PC12)injury induced by corticosterone(CORT)and its mechanism.METHODS PC12 cells were divided into normal group(nothing was processed),model group(CORT+untreated),ARC low dose group(CORT+50μmol/L ARC),and ARC high dose group(CORT+100μmol/L ARC).MTS assay was used to detect cell viability.LDH assay was used to detect LDH release rate.Annexin V staining method was used to detect the cell apoptosis rate.Western blotting was used to detect the expressions of apoptotic protein B lymphoblastoma-2 gene(Bcl-2),Bcl-2 associated X protein(Bax),cystein-asparate protease-3(Caspase-3)and high mobility group protein 1(HMGB1).RESULTS Compared with the normal group,the cell survival rate was significantly decreased(P<0.001),while the LDH release rate and cell apoptosis rate were significantly increased(P<0.001),and the expression level of Bcl-2 protein was decreased(P<0.001),the protein expression levels of Bax,Caspase-3 and HMGB1 were significantly increased in the model group(P<0.001).Compared with the model group,the cell survival rate was significantly increased after treatment with different concentrations of ARC(100,50μmol/L;P<0.001,P<0.01),the LDH release rate,apoptosis rate and necrosis rate were significantly decreased(P<0.001,P<0.01),the expression of Bcl-2 protein was significantly increased(P<0.001,P<0.05),and protein expression levels of Bax,Caspase-3 and HMGB1 were significantly decreased(P<0.001,P<0.01).CONCLUSION ARC has protective effect on CORT-induced PC12 injury,and its mechanism may be related to the regulation of apoptotic pathway to inhibit apoptosis and inhibit the transfer of HMGB1 to the cytoplasm.
作者
王雨
鲁京梅
赵新宇
金光男
郭佳晴
朴硕
彭娟
张美玲
徐翔
朴莲荀
WANG Yu;LU Jingmei;ZHAO Xinyu;JIN Guangnan;GUO Jiaqing;PIAO Shuo;PENG Juan;ZHANG Meiling;XU Xiang;PIAO Lianxun(Yanbian University College of Pharmacy,Yanji 133002,Jilin,China)
出处
《延边大学医学学报》
CAS
2022年第4期235-239,共5页
Journal of Medical Science Yanbian University
基金
国家自然基金项目(81960375)
吉林省大学生创新训练项目(202110184023)
延边大学博士启动基金(ydbq202218)
