摘要
目的观察链脲佐菌素(streptozotocin,STZ)诱导的实验性糖尿病对APP/PS1转基因小鼠脑组织中糖原合成酶-3α(GSK-3α)蛋白活性的影响。方法 3月龄APP/PS1转基因小鼠腹腔内注射STZ建立实验性糖尿病模型。使用电子天平和便携式血糖仪定期检测小鼠体重和血糖的变化。应用免疫组织化学方法和western blotting方法检测AD转基因小鼠脑组织中p-GSK-3α和GSK-3α的蛋白表达。结果动物饲养20W后,与APP/PS1转基因小鼠比较,STZ组转基因小鼠体重下降(P<0.05),血糖则明显升高(P<0.01),提示糖尿病模型诱导成功。Western blotting结果显示,STZ组APP/PS1转基因小鼠脑内p-GSK-3α蛋白表达水平较APP/PS1转基因小鼠明显降低(P<0.01),而总GSK-3α蛋白没有变化(P>0.05),两者的比值p-GSK-3α/GSK-3α下降49%(P<0.01)。免疫组化染色显示,STZ组转基因小鼠大脑皮层神经元内p-GSK-3α阳性表达明显低于转基因小鼠。结论 STZ上调APP/PS1转基因小鼠脑组织内GSK-3α蛋白活性。
Objective To investigate the effect of streptozotocin （STZ） on activity of GSK-3αprotein in APP/PS1 transgenic mice.Methods Three-month-old APP/PS1 mice were intraperitoneally injected with STZ to form experimental diabetes mellitus model.The body weight and blood glucose levels of the mice were monitored using electronic balance and portable blood glucose meter.The expressions of p-GSK-3αand GSK-3αwere detected by western blotting and immunohistochemisty.Results STZ-treated mice had lower body weights （P〈0.05） and higher levels of blood glucose compared with the control group （P〈0.05） twenty weeks after injection of STZ.Western blotting showed that STZ treatment significantly downregulated the level of p-GSK3α（P〈0.01） in brain of APP/PS1 mice,but with no change for the total protein level of GSK3α（P〉0.05）,the ratio of p-GSK3α/GSK3α was significantly reduced by 49% in STZ treated mice than in untreated （P〈0.01）.Immunohistochemistry indicated that the immunoreactivity of p-GSK-3αwas located in the cortex of STZ-treated mice.Conclusions STZ enhanced the activity of GSK-3α in APP/PS1 transgenic mouse brain.
出处
《解剖科学进展》
CAS
2011年第4期372-374,377,共4页
Progress of Anatomical Sciences
