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作 者:刘若海[1] 王颖[2] 吴文俊[3] 金芃芃[2] 余立群[2] 曹红[2] 李旭[2]
机构地区:[1]温州医科大学附属第二医院麻醉科,浙江温州325027 [2]温州医科大学仁济学院生理学教研室,浙江温州325035 [3]温州医科大学附属第一医院内分泌科,浙江温州325035
出 处:《中国病理生理杂志》2016年第10期1757-1762,共6页Chinese Journal of Pathophysiology
基 金:浙江省教育厅一般科研项目(No.Y201431185)
摘 要:目的:观察1型糖尿病(DM)大鼠给予高盐饮食后内皮细胞功能障碍的可能机制。方法:SD大鼠(150-180 g)60只,腹腔注射链唑霉素(70 mg/kg),3 d后空腹血糖≥16.7 mmol/L为1型DM大鼠。正常大鼠和DM大鼠分别给予正常饮食和高盐饮食(8%Na Cl)6周。检测肠系膜动脉舒张功能,Western blot技术检测血管中Akt、内皮型一氧化氮合酶(e NOS)、caveolin-1(Cav-1)等蛋白的水平。结果:高盐饮食DM大鼠收缩压显著高于DM组,其肠系膜动脉乙酰胆碱和胰岛素的舒张作用显著下降(P〈0.01)。Akt、p-e NOS和NO水平均显著低于DM组(P〈0.01),Cav-1显著增高(P〈0.01)。结论:1型糖尿病大鼠高盐饮食血管功能障碍可能与抑制内皮细胞Akt激活及增强Cav-1表达导致的e NOS活性下降有关。AIM: To investigate the underlying mechanisms responsible for endothelial dysfunction of type 1 diabetes mellitus (DM) rats fed with high-salt diet.METHODS:Type 1 DM was induced by intraperitoneal injection of streptozotocin (70 mg/kg).Normal and diabetic rats were fed high-salt food (HS, 8% NaCl) and standard food for 6 weeks, respectively.Isometric tension of the mesenteric arteries were measured .The expression of Akt , endothelial nitric oxide synthase (eNOS) and caveolin-1 (Cav-1) was examined by Western blot .RESULTS:The rats in DM+HS group exhibited more pronounced impairment of vasorelaxation to acetylcholine and insulin compared with either DM group or HS group (P〈0.01).Akt and eNOS phosphorylation levels, and nitric oxide (NO) concentration in DM +HS group were significantly lower than those in DM group (P〈0.01).The level of Cav-1 in DM+HS group was significantly higher than that in DM group and HS group .CONCLUSION:Impaired endothelial Akt activation , increased Cav-1 expression and resultant decreased eNOS activation contribute to aggravate high-salt dietinduced endothelial dysfunction and hypertension in DM rats.
关 键 词:高盐饮食 糖尿病 CAVEOLIN-1 内皮型一氧化氮合酶 肠系膜动脉
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