摘要
目的探讨高级糖基化终末产物受体(RAGE)、血管紧张素Ⅱ受体-1(AT1R)在糖尿病(DM)脑组织病变的可能机制。方法 20只SD大鼠随机分为对照组和糖尿病组。第16周末行脑磁共振检查;于20周末处死大鼠,留取脑组织标本,行HE染色检测其病理学改变;采用免疫组化SP法检测脑组织RAGE、AT1R、基质金属蛋白酶9(MMP9)及胶原纤维酸性蛋白(GFAP)的表达,并进行相关性分析。结果糖尿病组大鼠磁共振显示大脑白质病变,T1WI低信号、T2WI高信号;组织病理学显示脑组织小血管周隙明显增宽,未见坏死及炎细胞浸润;糖尿病组脑组织RAGE、AT1R、MMP9阳性细胞数较对照组明显升高,差异有统计学意义(P<0.05),GFAP阳性细胞数无明显变化;糖尿病组脑组织RAGE、AT1R呈正相关(P=0.015);糖尿病组大鼠MMP9与RAGE、AT1R呈正相关(P=0.001,0.037)。结论 DM大鼠白质病变的病理表现是脑小血管周围的水肿,其机制可能与RAGE、AT1R及MMP9表达有关。
Objective To investigate possible mechanism on receptor for advanced glycation and angiotensin Ⅱ type 1 receptor ( AT1 R) of brain tissue lesion of diabetic rats. Methods end products ( RAGE ) 20 SD rats were randomly devided into the control group and diabetic group. Brain MRI examination was checked in the 16th weekend; Rats were killed and brain tissue specimens were obtained in the 20th weekend, pathological changes were detected with HE staining. The proteins expression of RAGE, AT1 R, MMP9 and GFAP in brain tissue were detected by immunohistochemical staining, and sequently the datas in the experiment were made correlation analysis. Results White matter lesions were seen T1WI-low signal and T2WI-high signal in MRI; It were presented that a small perivascular was significantly widened, no necrosis or inflammatory cell infiltration in brain tissue with diabetic group rats;RAGE, AT1 R, MMP9 positive cells with diabetic group rats was significantly higher than those in the control group, which the difference was statistically significant ( P 〈 0. 05 ), but GFAP-positive cells was no significant between the two groups (P 〉 0. 05 ) ;RAGE and AT1 R was positively correlated (P = 0. 015 ) ; MMP9 concentration was positively correlated with RAGE and AT1R respectively (P = 0. 001,0. 037 ) in the diabetic group rats. Conclusion Brain edema is observed around the small blood vessels on white matter lesions of diabetic rats, and the mechanism may be involved in the expression of RAGE, AT1R and MMP9.
出处
《安徽医科大学学报》
CAS
北大核心
2012年第6期627-630,共4页
Acta Universitatis Medicinalis Anhui