摘要
目的从糖尿病大鼠肾脏PKC活性改变入手,研究氨基胍(AG)对糖尿病大鼠肾脏的保护作用。方法将48只雄性Wistar大鼠随机分为四组,给予C组、D组大鼠氨基胍治疗24周,分别测定治疗8周、12周、24周时大鼠的体重、血糖、糖化血红蛋白(HbA1c)和PKC活性,各组治疗结果进行比较。结果治疗8周、12周、24周后,测得糖尿病组大鼠血糖、HbA1c和肾小球PKC活性均升高,氨基胍治疗组糖尿病大鼠的血糖、HbA1c及体重变化无显著性差异,但在治疗24周时PKC活性恢复正常。结论氨基胍阻止或延缓糖尿病相关的肾脏损害可能涉及多种机制,通过抑制蛋白激酶C通路是其机制之一。PKC活性升高在糖尿病肾病进展中起重要作用,氨基胍可下调PKC活性并可能是一种新的PKC抑制剂。
Objective： To explore the alteration of Protein Kinase C（PKC） activity in diabetic rats and the effect of aminoguanidine （AG） on the Protein Kinase C activity of diabetic glomerulopathy in STZ-induced diabetic rats. Methods 48 male Wistar rats were randomized into 4 groups o AG was administered to C and D groups. Blood glucose, HbAlc and PKC activity were measured and analysed in 8, （12） and 24 weeks. The results were compared with other groups. Results After treatment for 8, （12} and 24 weeks the levels of blood glucose, HbAlc and PKC activity were all significantly increased in diabetic rats. AG had no influence on the alteration of blood glucose, HbA1c and weight in diabetic rats, but could decrease the activity of PKC. Conclusion The rise of PKC activity plays one of important roles in the development of DN AG could reduce the PKC activity and it may be a novel inhibitor of protein kinase C.
出处
《泰山医学院学报》
CAS
2006年第1期10-13,共4页
Journal of Taishan Medical College
