心肌缺血再灌注损伤中信号分子p38MAPK作用的研究

发布时间：2018-07-29 18:49

【摘要】：目的：通过构建动物模型,研究信号分子p38MAPK在心肌缺血再灌注损伤中的作用,同时探讨p38MAPK抑制剂及蒙诺对心肌缺血再灌注损伤的作用及其与p38MAPK信号传导途径的关系。 方法：雄性SD大鼠随机分为5组(N组：假手术组；A组：单纯缺血组；B组：缺血再灌注组；C组：蒙诺干预+缺血再灌注组；D组：p38MAPK抑制剂干预+缺血再灌注组)。术前及术中监测心电图变化,C组用蒙诺进行干预,D组用抑制剂进行干预,余用生理盐水干预。造模完成后抽血进行心肌酶谱分析,并处死大鼠取心肌组织用PCR及免疫组化方法检测磷酸化p38MAPK (p-p38MAPK)的基因和蛋白表达。 结果：1.B组、C组及D组的血清CK、CKMB含量值较对照组(N组)均升高,D组和C组的含量值较B组降低,差异均极显著(P0.01)。2.B组p38MAPK基因的含量较N组升高,D组的含量较B组降低,差异均极显著(P0.01)。3.A组、B组、C组及D组的p-p38MAPK含量均高于N组,A组和D组含量低于B组,差异均极显著(P0.01)。 结论：心肌缺血再灌注可激活p38MAPK信号途径,活化的p38MAPK可减轻心肌再灌注损伤；福辛普利对心肌缺血再灌注损伤所起的保护作用可能与p38MAPK信号传导途径有关。
[Abstract]:Aim: to study the role of signal molecule p38MAPK in myocardial ischemia-reperfusion injury by establishing animal model, and to investigate the effect of p38MAPK inhibitor and monno on myocardial ischemia-reperfusion injury and its relationship with p38MAPK signal transduction pathway. Methods: male Sprague-Dawley rats were randomly divided into 5 groups (group N: sham operation group, group A: simple ischemia group, group B: ischemia reperfusion group, group C: monno intervention group, group D, intervention of p38 MAPK inhibitor, intervention group, ischemia and reperfusion group). Electrocardiogram changes were monitored before and during operation. Group C was treated with monno, group D with inhibitor, and group C with normal saline. After the model was made, the myocardial enzyme analysis was performed, and the expression of phosphorylated p38MAPK (p-p38MAPK) gene and protein were detected by PCR and immunohistochemistry. Results 1. Compared with the control group (N group), the level of p38MAPK MB in group C and D was significantly higher than that in group B (P 0.01). The content of p38MAPK gene in group B was significantly higher than that in group D and group C, and the content of p38MAPK gene in group B was significantly lower than that in group B (P 0.01), and the level of p38MAPK in group B was significantly lower than that in group B (P < 0.05). The content of p-p38MAPK in group B, C and D was significantly higher than that in group N, group A and group D, and the difference was very significant (P0.01). 3. The content of p-p38MAPK in group A was significantly higher than that in group B (P0.01), and the content of p-p38MAPK in group D was lower than that in group B (P0.01). Conclusion: myocardial ischemia-reperfusion can activate p38MAPK signal pathway and activated p38MAPK can reduce myocardial reperfusion injury, and the protective effect of fosinopril on myocardial ischemia-reperfusion injury may be related to the p38MAPK signal transduction pathway.
【学位授予单位】：石河子大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363

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