丹酚酸B对间歇性高糖诱导的JNK活化和INS-1细胞凋亡的影响  

Effect of salvianolic acid B on intermittent high glucose induced JNK activation and INS-1 cell apoptosis

作　　者：郑书国[1] 朱元美[1] 陶善珺 郑浩文[1] 任尤楠 赵梦秋 杨解人[1] 吴元洁[3] 

机构地区：[1]皖南医学院药理教研室,安徽芜湖241002 [2]安徽人口职业学院基础医学教研室,安徽池州247009 [3]安徽中医药大学中医基础学教研室,安徽合肥230038

出　　处：《中国药理学通报》2017年第1期68-73,共6页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81102626);安徽省高校省级自然科学研究重点项目(No KJ2015A192);皖南医学院大学生科研资助金资助项目(No WK2015S26)

摘　　要：目的观察丹酚酸B(Salvianolic acid B,Sal B)对间歇性高糖诱导的大鼠胰岛素瘤细胞(INS-1)c-Jun氨基末端激酶(JNK)活化和细胞凋亡的影响。方法 INS-1细胞与丹酚酸B预孵24 h后暴露于间歇性高糖(11.1 mmol·L^(-1)12 h,33.3 mmol·L^(-1)12 h)72 h。MTT法测定细胞活力,ELISA法测定葡萄糖刺激的胰岛素分泌能力,荧光探针DCFH-DA检测细胞内活性氧(ROS)水平,流式细胞术检测细胞凋亡水平,Western blot法检测胰十二指肠同源盒-1(PDX-1)蛋白表达和JNK活化水平。结果丹酚酸B可明显减轻间歇性高糖诱导的INS-1细胞损伤和凋亡(P<0.05,P<0.01),提高葡萄糖刺激的胰岛素分泌能力(P<0.05,P<0.01);与丹酚酸B预孵可明显降低细胞内ROS水平、抑制JNK活化,并提高PDX-1蛋白表达水平(P<0.05,P<0.01)。结论丹酚酸B可有效减轻间歇性高糖诱导的INS-1细胞损伤和凋亡,提高胰岛素分泌水平,其机制可能与降低细胞内ROS水平、抑制JNK活化和上调PDX-1蛋白表达有关。Aim To investigate the effect of salvianolic acid B（ Sal B） on c-Jun N-terminal kinase（ JNK） activation and apoptosis of INS-1 cells induced by intermittent high glucose. Methods INS-1 cells were preincubated with Sal B for 24 h,followed by exposure to intermittent high glucose（ IHG,11. 1 mmol · L^（-1）12 h,33. 3 mmol·L^（-1）12 h） for 72 h. Cell viability was assessed by MTT assay and cell apoptosis was evaluated by flow cytometry. Glucose induced insulin secretion capacity and intracellular reactive oxygen species（ ROS） contents were measured by enzyme linked immunosorbent assay（ ELISA） and a fluorescent probe DCFH-DA,respectively. Levels of JNK activation and PDX-1 protein expression were determined by Western blot analysis. Results Sal B significantly alleviated IHG-induced cell injury and apoptosis,with glucose induced insulin secretion capacity improved evidently（ P 0. 05 or P 0. 01）. Preincubation with Sal B notably decreased intracellular ROS and JNK activation in INS-1 cells,while the level of PDX-1 protein was increased markedly（ P 0. 05 or P 0. 01）. Conclusion Sal B is capable of ameliorating IHG-induced cell injury and apoptosis in INS-1 cells,which might be derived from suppression of JNK activation and upregulation of PDX-1 protein expression.

关 键 词：丹酚酸B INS-1细胞 2型糖尿病 间歇性高糖 JNK 凋亡 

分 类 号：R-332[医药卫生] R284.1