姜黄素对糖尿病大鼠大脑海马神经元的作用研究

Effect of Curcumin on hippocampal neurons in diabetic rats

目的观察姜黄素(Curcumin,Cur)对STZ诱导的2型糖尿病大鼠大脑海马神经元的影响。方法雄性SD大鼠随机分为3组:正常对照组(Con组),高糖高脂饮食结合链脲佐菌素(STZ)诱导的2型糖尿病模型组(DM组)和给予姜黄素处理的糖尿病组(DM+Cur组)。免疫印迹法(WB法)检测大鼠大脑海马凋亡相关蛋白Bcl-2和Bax的蛋白含量;免疫组织化学法(IHC法)检测凋亡执行者caspase-3在大鼠大脑海马各区中的表达情况。结果大鼠给予高糖高脂饮食一个月后,腹腔注射STZ可诱导大鼠血糖升高,继续给予高糖高脂饮食,大鼠出现类似于2型糖尿病的症状,通过WB检测,DM组大鼠海马的Bcl-2/Bax比值较Con组明显下降(P<0.05),而给予姜黄素处理16周后的DM+Cur组大鼠可明显增强抗凋亡蛋白Bcl-2的表达而减弱促凋亡蛋白Bax的表达,两者比值增大(P<0.05);另外,通过IHC法检测发现,DM组大鼠海马各区的caspase-3阳性表达明显增多,而DM+Cur组可减弱caspase-3的阳性表达。结论高糖高脂饮食结合STZ腹腔注射可诱导出2型糖尿病大鼠模型,姜黄素能通过调控DM大鼠海马凋亡相关蛋白的表达而发挥保护作用。

Objective To investigate the effect of curcumin on hippocampal neurons of STZ-induced type 2diabetic rats.Methods Male SD rats were randomly divided into three groups:normal control group(Con),high-carbohydrate and high-fat diet combined with streptozotocin(STZ)induced type 2diabetic model group(DM)and the diabetic group treated with curcumin(DM + Cur).Apoptosis related proteins Bcl-2and Bax in rat brain hippocampu were detected by western blotting(WB);and apoptosis executor caspase-3was detected by immunohistochemistry(IHC).Results The blood glucose was escalated after feeding rats with high-carbohydrate and high-fat diet a month and intraperitoneal injection of STZ.Keeping on giving this diet to rats,induced the symptoms similar to type 2diabetes.WB testing showed that the ratio of Bcl-2/Bax in the DM group was significantly decreased compared to that of the Con group(P<0.05),while the rats of diabetic group treated with curcumin 16weeks(DM + Cur group)showed significantly enhanced expression of anti-apoptotic protein Bcl-2and weakened expression of apoptotic protein Bax,and the ratio of them was increased(P<0.05).In addition,IHC detection showed that caspase-3expression in rat hippocampus was significantly increased in the DM group,but reduced in the DM + Cur group.Conclusion High-carbohydrate and high-fat diet combined with intraperitoneal injection of STZ can induce rat models of type 2diabetes,and curcumin can play aprotective role by regulating the expression of apoptosis-related proteins in DM rat hippocampus.