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作 者:刘晓敏[1] 胡向阳[2] 余锋[1] 陈银河[3] 邓大丽
机构地区:[1]安徽医科大学附属省立医院神经内科,合肥230001 [2]安徽医科大学第一附属医院病理科,合肥230022 [3]安徽医科大学第一附属医院骨科,合肥230022 [4]安徽医科大学附属省立医院脑立体定向神经外科研究所,合肥2300013
出 处:《安徽医科大学学报》2013年第10期1170-1173,共4页Acta Universitatis Medicinalis Anhui
摘 要:目的探讨血管紧张素Ⅱ受体-1(AT1R)、血管紧张素Ⅱ受体-2(AT2R)、高级糖基化终末产物受体(RAGE)在糖尿病大鼠脑组织损伤中的可能作用。方法 40只SD大鼠随机均分为糖尿病组和对照组。链脲佐菌素注射后12周末处死大鼠,留取脑组织标本,行HE染色观察其病理学改变,采用免疫组化Evision二步法检测脑组织中AT1R、AT2R、RAGE及基质金属酶9(MMP9)的表达,并将糖尿病组AT1R、AT2R、RAGE、MMP9进行相关性分析。结果糖尿病组较对照组大鼠脑组织病理学显示脑小血管周隙明显增宽,但两组脑组织均无炎细胞浸润;糖尿病组大鼠脑组织AT1R、AT2R、RAGE、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);糖尿病组大鼠AT2R与MMP9、RAGE、AT1R均呈正相关(P<0.05),AT1R与MMP9、RAGE呈正相关(P<0.05),MMP9与RAGE呈正相关(P=0.001)。结论糖尿病大鼠脑组织存在水肿,提示有血脑屏障异常,其机制可能与AT1R、RAGE、MMP9的过度表达或AT2R的激活以及它们之间的相互作用有关。Objective To investigate possible mechanism on angiotensin 11 type 1 receptor( AT1 R), angiotensin II type 2 reeeptor(AT2R), receptor for advanced glycation end products(RAGE) of blood-brain barrier lesion of diabetic rats. Methods SD rats were randomly devided into the diabetic group and the control group. Rats were killed and brain tissue specimens were obtained in the 12th weekend after streptozocin injection. Pathological changes were detected with HE staining; the proteins expression of ATIR, AT2R, RAGE and MMP9 in brain tissue were tested by immunohistochemical staining, and sequently the data in the experiment were made correlation analysis. Results It presented that diabetic group rats blood-brain barrier were lesioned, but without inflammatory cell infiltrated in brain tissues of the two groups. AT1 R, AT2R, RAGE, MMP9 positive cells in the diabetic group rats were significantly higher than those in the control group, with the difference being statistically significant (P 〈 0.05). AT2R was positively correlated with MMP9, RAGE and ATIR respectively (P = 0. 025,0. 002, 0. 001 ) ; AT1R was positively correlated with MMP9 and RAGE respeetively(P = 0. 041, 0. 026); MMP9 and RAGE was positively correlated( P =0. 001 ) in the diabetic group rats. Conclusion There is brain edema around the small blood vessel of brain tissues, which suggests that blood-brain barrier permeability is increased in diabetic rats. The mechanism may be the over-expression of ATIR, RAGE, MMP9 or activation of AT2R and interreaetion among them.
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