桑白皮含药血清抑制高脂高糖诱导的胰岛β细胞凋亡的分子机制

Molecular Mechanism of Cortex Mori Radicis Serum Inhibiting Apoptosis of Islet β Cells Induced by Palmitic Acid and High Glucose

目的观察桑白皮含药血清对高脂高糖诱导的胰岛β细胞凋亡的抑制效应,探讨桑白皮治疗糖尿病的分子机制。方法制备桑白皮药物血清并干预胰岛β细胞,分为正常组、高脂高糖组、药物血清组;MTT法检测细胞活性,western blot检测各组细胞凋亡蛋白Bax和Bcl-2表达水平,FCM流式细胞术检测细胞凋亡率。结果根据细胞活性检测选择10倍药物血清细胞。FCM流式细胞术结果显示:与正常组比较,高脂高糖组细胞凋亡率高(<0.05);与高脂高糖组比较,药物血清组细胞凋亡率明显降低(<0.05)。蛋白免疫印迹结果显示:与正常组比较,高脂高糖组Bcl-2表达减少而Bax表达增加;与高脂高糖组比较,Bcl-2表达增加而Bax表达减少(<0.05)。结论桑白皮药物血清可抑制高脂高糖诱导的胰岛β细胞凋亡,其抑制作用是通过调节Bax和Bcl-2表达实现的。

Objective To investigate the molecular mechanism of Cortex Mori Radicis serum inhibiting apoptosis of islet β cells induced by palmitic acid（PA） and high glucose. Methods The serum of Cortex Mori Radicis was prepared and the islet β cells were intervened. The cells were divided into normal group,PA and high glucose group and drug sera group;cell activity was detected by MTT method;Western blot was used to detect the expression of Bax and Bcl-2 in each group of apoptotic proteins;FCM flow cytometry was used to detect the apoptosis rate. Results Sera cells were selected based on cell activity detection. The results of FCM flow cytometry showed that： compared with normal group, the apoptosis rate of PA and high glucose group was higher（P〈0.05）; compared with PA and high glucose group, the apoptosis rate of drug sera group decreased significantly（P〈0.05）; the results of protein immunoblotting showed that： compared with normal group, the expression of Bcl-2 decreased and BAX increased in PA and high glucose group（P〈0.05）; compared with PA and high glucose group, the expression of Bcl-2 increased and BAX decreased（P〈0.05）. Conclusion Cortex Mori Radicis serum can inhibit the apoptosis of islet β cells induced by PA and high glucose,and its inhibiting effect is achieved by regulating the expression of Bax and Bcl-2.