橙皮苷对高脂高糖诱导胰岛 β 细胞损伤的保护作用

目的探讨橙皮苷(hesperidin,HSD)对于高脂高糖诱导小鼠胰岛β细胞损伤的保护作用及机制。方法HSD预处理后,高脂高糖处理MIN6细胞。CCK-8法、Hoechst 33258荧光染色法检测MIN6细胞增殖与凋亡;Western blot检测Bax、Bcl-2的表达;RT-PCR检测炎症因子TNF-α、IL-1β的表达;ELISA检测小鼠胰岛的胰岛素分泌功能。结果高脂高糖培养抑制MIN6细胞增殖,诱导细胞凋亡,降低Bcl-2/Bax比值,增加炎症因子TNF-α、IL-1β的表达并且抑制了小鼠胰岛的胰岛素分泌;当HSD预处理后,MIN6细胞活力增加,Bcl-2/Bax比值增加,炎症因子TNF-α、IL-1β的表达有不同程度的降低,小鼠胰岛的胰岛素分泌增加。结论HSD减少了高脂高糖诱导的小鼠胰岛β细胞株MIN6细胞凋亡和炎症因子分泌,改善小鼠胰岛素分泌。

The protective effect of hesperidin on injury induced by glucolipotoxicity in islet beta cells

Aim To investigate the protective effect of hesperidin(HSD)on the injury of mouse pancreatic beta cells induced by high glucose and fatty acid and the underlying mechanism.Methods MIN6 cells were treated with high glucose and fatty acid after pretreatment of HSD.Cell counting kit-8(CCK-8)and Hoechst 33258 fluorescence staining were used to determine the proliferation and apoptosis of MIN6 cells.Western blot was used to detect the expressions of apoptosis-related proteins Bcl-2 and Bax.RT-PCR was used to detect the expressions of inflammatory factors tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β).ELISA was used to test the insulin secretion of pancreatic islets.Results High glucose and fatty acid decreased the ratio of Bcl-2/Bax,increased the expression of inflammatory factors TNF-αand IL-1βand inhibited the insulin secretion of mouse pancreatic islets.After pretreatment of HSD,the cell viability and Bcl-2/Bax ratio of MIN6 increased,the expressions of inflammatory factors TNF-αand IL-1βdecreased,and the insulin secretion of mouse pancreatic islets increased.Conclusions HSD could resist the apoptosis of mouse pancreatic isletβcell line MIN6 induced by high fat and high glucose,reduce the secretion of inflammatory factors and improve the insulin secretion of pancreatic islets.