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缺血后处理对糖尿病大鼠脑组织 NO及 NOS 含量的影响
引用本文:卢英云,;赵光军,;杨艳娜,;刘颖,;王翠兰. 缺血后处理对糖尿病大鼠脑组织 NO及 NOS 含量的影响[J]. 当代医师, 2014, 0(6): 731-733
作者姓名:卢英云,  赵光军,  杨艳娜,  刘颖,  王翠兰
作者单位:[1]山东省交通医院血栓科,济南250031; [2]济南军区政治部门诊部;,济南250031; [3]济南市中心医院呼吸科;,济南250031; [4]山东大学齐鲁医院神经内科,济南250031;
基金项目:山东省自然科学基金(Y2007C087)
摘    要:目的:探讨缺血后处理对糖尿病大鼠脑组织一氧化氮( NO)及一氧化氮合成酶( NOS)含量的影响。方法将30只Wistar大鼠(180-200 g)按随机数字表法分为空白组、缺血组和缺血后处理组。均经一次性链脲佐菌素(STZ)腹腔注射建立糖尿病大鼠模型。缺血组和缺血后处理组大鼠结扎颈总动脉,造脑缺血模型,缺血后处理组对大鼠进行缺血后处理。 HE染色观察各组大鼠脑组织形态学变化,ELISA法检测大鼠血清中NO及NOS各亚型的含量变化,同时免疫印迹( Western blot )法检测脑组织中NOS蛋白的表达情况。结果缺血后处理组大鼠脑组织缺损降低,神经元细胞增多,与缺血组相比,缺血后处理组iNOS明显下降,差异具有统计学意义( P <0.05),而与空白组大鼠差异无统计学意义( P >0.05)。 WB结果显示,缺血后处理大鼠中iNOS的表达明显弱于缺血组( P <0.05),与空白组差异无统计学意义( P >0.05)。结论缺血后处理对糖尿病大鼠脑组织具有一定的保护作用,可能是通过抑制NOS特别是iNOS的活性,达到治疗的作用。

关 键 词:再灌注损伤  预防和控制  糖尿病  一氧化氮  代谢  一氧化氮合酶  代谢  大鼠  Wistar

Effects of ischemic postconditioning on nitric oxide and nitric oxide synthase in diabetic rat brain tissues
Affiliation:Lu Yingyun, Zhao Guangjun, Yang Yanna, Liu Ying, Wang Cuilan( Department of Thrombosis, Shandongiiaotong Hospital, Jinan 250031, China)
Abstract:Objective To investigate effects of ischemic postconditioning on the nitric oxide ( NO) and nitric oxide synthase ( NOS) in diabetic rat brain tissues .Methods Thirty Wistar rats were diabetic models induced by intraperitoneal injuction of stepto-zotocin (STZ), and randomly divided into three groups: Control group (normal, diabetic), cerebral ischemia group, and ischemic postconditioning ( I-POST) group.The rats of cerebral ischemia group and ischemic postconditioning group were made model of cere -bral ischemia by ligation carotid artery .Hematoxylin-eosin ( HE) was used to observe their pathological changes in control and diabetic groups.Enzyme-linked immunosorbent assay ( ELISA) method was used to detect the expression and changes of NO and NOS in the sera in each group .Western Blot method was used to investigate the expression and changes of NOS in the retinal tissues in each group .Results For I-POST group , brain tissue defects were decreased , neuronal cells were increased , serum inducible NOS ( iNOS) content was significantly lower than endothelial NOS (eNOS) and neuronal NOS (nNOS) ( P 〈0.05), brain tissue iNOS expression was significantly weaker than ischemia group ( P 〈0.05 ) and was not different from normal group ( P 〉0.05 ) .Conclusions Is-chemic postconditioning can protect the brain tissue of diabetic rats by inhibiting NOS activity especially iNOS .
Keywords:Reperfusion injury/prevention & control  Diabetes mellitus  Nitric oxide/metabolism  Nitric oxide synthase/metabolism  Rats, Wistar
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