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【摘要】：目的：通過構建動物模型,研究信號分子p38MAPK在心肌缺血再灌注損傷中的作用,同時探討p38MAPK抑制劑及蒙諾對心肌缺血再灌注損傷的作用及其與p38MAPK信號傳導途徑的關系。 方法：雄性SD大鼠隨機分為5組(N組：假手術組；A組：單純缺血組；B組：缺血再灌注組；C組：蒙諾干預+缺血再灌注組；D組：p38MAPK抑制劑干預+缺血再灌注組)。術前及術中監(jiān)測心電圖變化,C組用蒙諾進行干預,D組用抑制劑進行干預,余用生理鹽水干預。造模完成后抽血進行心肌酶譜分析,并處死大鼠取心肌組織用PCR及免疫組化方法檢測磷酸化p38MAPK (p-p38MAPK)的基因和蛋白表達。 結果：1.B組、C組及D組的血清CK、CKMB含量值較對照組(N組)均升高,D組和C組的含量值較B組降低,差異均極顯著(P0.01)。2.B組p38MAPK基因的含量較N組升高,D組的含量較B組降低,差異均極顯著(P0.01)。3.A組、B組、C組及D組的p-p38MAPK含量均高于N組,A組和D組含量低于B組,差異均極顯著(P0.01)。 結論：心肌缺血再灌注可激活p38MAPK信號途徑,活化的p38MAPK可減輕心肌再灌注損傷；福辛普利對心肌缺血再灌注損傷所起的保護作用可能與p38MAPK信號傳導途徑有關。
[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.
【學位授予單位】：石河子大學
【學位級別】：碩士
【學位授予年份】：2011
【分類號】：R363

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