摘要
目的 探讨前体蛋白 N端 11肽神经营养作用的机理。 方法 用链脲佐菌素诱发小鼠糖尿病模型。小鼠分为 :正常对照组 (C组 )、糖尿病对照组 (DM组 )、UPAN治疗组 (U PAN+DM组 )。 UPAN +DM组于糖尿病造模后 2周起至 STZ给药后 4周皮下注射 UPAN,每次 0 . 2 0μg,1次/ d。造模成功 4周后 ,将动物处死 ,行灌注固定 ,取脑组织作冰冻切片 ,进行神经生长因子 (NGF)、神经元纤维蛋白 (NF)及早老蛋白 - 1(PS- 1)免疫组化染色。 结果 UPAN可恢复或部分恢复糖尿病小鼠脑海马神经元 NGF、NF及 PS- 1中的 141(N端 2 5 8- 2 77)表达。 结论 U PAN对糖尿病小鼠的神经元退行性变可能有改善作用 ,PS- 1N端和 C端增加的意义尚需进一步研究。
Objective To study the changes in NGF?NF and PS 1 in the hippocampus of diabetic mice, and to observe the effects of UPAN on the foregoing changes. UPAN is the 63 73 peptide sequence of APP695. Methods Mouse diabetic model was produced with streptozotocin. UPAN was injected subcutaneouly into diabetic mice with dose of 0. 20 ug/per mouse/per day after two weeks . Four weeks later, fixative was injected intravascularly into the mouse. After the brain was fixed, cryostat sections of 40 micrometer thickness were prepared and immunohistochemical staining for NGF?NF and PS 1 were made. Results The use of UPAN could restore protein expression in the NGF?NF and 258 277 peptide sequence of PS 1(141)( P< 0.01). Conclusion UPAN may improve the neurodegenerative changes of diabetic mice.The significance of the increase of the N terminal fragment and the C terminal fragment is to be studied.
出处
《中国糖尿病杂志》
CAS
CSCD
2002年第3期152-154,共3页
Chinese Journal of Diabetes
基金
国家科技部 973课题资助项目 ( G2 0 0 0 0 5 70 10 )
