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机构地区:[1]河北省唐山市丰润区人民医院普外科,064000 [2]河北联合大学解剖学教研室
出 处:《山西医药杂志》2016年第11期1253-1255,共3页Shanxi Medical Journal
基 金:河北省唐山市科学技术研究与发展计划(111302069a)
摘 要:目的观察P38丝裂原活化蛋白激酶信号通路抑制剂SB203580对急性重症胰腺炎(SAP)大鼠大脑皮层诱导型一氧化氮合酶(iNOS)蛋白表达的影响。方法将45只SD大鼠按随机数字法分3组。模型组:将5%牛磺胆酸钠经胰胆管逆行注入胰腺制备;抑制剂组:造模后于大鼠尾静脉注射SB203580;对照组开腹后翻动胰腺数次立即缝合腹壁,尾静脉注射0.9%氯化钠注射液。造模成功后24h,检测血清淀粉酶;应用免疫组织化学、蛋白印迹法观察及检测各组神经元中iNOS和磷酸化P38表达的变化,并进行图像分析和统计学处理。结果模型组大鼠p-P38、iNOS阳性神经元显著增加及蛋白水平升高;给予注射SB203580后,抑制剂组较模型组均明显减轻(P<0.05)。结论 P38丝裂原活化蛋白激酶信号通路抑制剂SB203580具有调控SAP大鼠大脑皮层iNOS蛋白表达的作用,减轻神经元的变性丢失。Objective To investigate the effect of P38 mitogen-activated protein kinase signaling pathway inhibitor SB203580 on the expression of inducible nitric oxide synthase(iNOS)in cortical neurons of the rats model of severe acute pancreatitis(SAP).Methods Forty-five healthy male rats were randomly divided into 3groups.model group:the rats were induced by retrograde injection 5%sodium taurocholate into the pancreatobiliary duct;inhibitor group:the rats were induced by injection SB203580 via the tail;control group:after laparotomy the rat pancreas were flipped several times and sutured immediately abdominal wall,which were injected with saline via the tail.After 24 hours,serum amylase were measured by immunohistochemistry and Western blotting.Each group of neurons is observed and detected change of iNOS and phosphorylation of P38 expression with the image analysis and statistical processing.Results The number of iNOS and phosphorylated P38 immunoreactive cells and their protein level in the cortical increased markedly in model group.After giving SB203580,the above changes were alleviated obviously.Conclusion In the rats model of SAP,P38mitogen-activated protein kinase signaling pathway regulates the expression of iNOS in cortical neurons.Inhibition of this pathway has a neuro-protective effect in rats with SAP.
关 键 词:胰腺炎 脑损伤 P38丝裂原活化蛋白激酶类 一氧化氮合酶
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