摘要
目的:观察糖尿病大鼠肾脏的蛋白质组,进一步探讨糖尿病引起肾脏病变的可能机制。方法:采用链脲菌素(STZ)诱发Wistar大鼠产生高血糖,建立1型糖尿病大鼠模型。用固相pH梯度双向凝胶电泳(2D-PACE)分离糖尿病大鼠与正常大鼠肾脏的蛋白质。考马斯亮蓝染色凝胶后,用ImageMaster 2D Platinum计算机软件进行图像分析。结果:图像分析测得2块大胶的匹配率达64%,在等电点3~10、分子量14.4~97.4kD分离得到实验组大鼠肾脏的蛋白质点约1073个,对照组大鼠的蛋白质点约1059个,其中至少70个蛋白点在两组肾脏间有2倍以上量变。结论:实验组大鼠肾脏蛋白质表达发生变化,差异蛋白质点的进一步研究有助于探讨糖尿病肾病的发病机制。
Objective: To explore the possible mechanism for diabetes mellitus (DM) causing nephropathy by examining the protein difference in kidney between diabetic rats and normal rats. Methods: DM rat models were established successfully by streptozocin (STZ) injection which caused high level of blood glucose in Wistar rats. The proteins in kidney of DM rats and normal rats were analyzed with two-dimensional gel electrophresis and imaging analysis. Results: The ratio of matched protein spots between gels of DM rats and normal rats was up to 64%. 1 059 and 1 073 protein spots with a molecular mass between 14.4 -97.4 kD and isoelectric points (pI) range of 3 - 10 were catalogued from co-stained gels. At least 70 proteins were up-regulated or down-regulated by tween two groups. Conclusion: The different expression of protein profile may be an over two folds beunderlying course of diabetic nephropathy.
出处
《贵阳医学院学报》
CAS
2007年第1期42-44,共3页
Journal of Guiyang Medical College