摘要
目的通过主动脉根部模拟冠状动脉内给药,探讨盐酸法舒地尔后适应对大鼠急性心肌缺血再灌注损伤的保护机制。方法选择SD大鼠30只,随机分为假手术组、缺血再灌注组、缺血后适应组、法舒地尔组、法舒地尔+LY294002组(LY294002组),每组6只。各组于再灌注180min后处死大鼠,取心肌组织用Western blot方法测定Bcl-2、Bax、caspase-3、蛋白激酶B(Akt)及磷酸化Akt的表达。结果与缺血再灌注组比较,缺血后适应组和法舒地尔组Bcl-2表达明显升高,Bax、caspase-3表达明显降低(P<0.05)。与法舒地尔组比较,LY294002组Bcl-2表达明显降低,Bax、caspase-3表达明显升高(P<0.05)。与缺血再灌注组和LY294002组比较,法舒地尔组磷酸化Akt表达明显升高(P<0.05)。结论盐酸法舒地尔后适应的机制可能与激活磷脂酰肌醇3-激酶-Akt传导通路有关。
Objective To study the mechanism of fasudil hydrochloride postconditioning in protec- ting rats against myocardial ischemia/reperfusion （I/R） injury. Methods Thirty SD rats were randomly divided into sham operation group, I/R group, ischemic postconditioning group, fasudil hydrochloride group and fasudil hydrochloride＋LY294002 group（6 in each group）. Th rats were sacrificed 180 minutes after reperfusion. Expressions of Bcl-2,Bax, caspase 3, Akt and P-Akt in myocardial tissue were detected by Western blot. Results The Bcl-2 expression level was signifi- cantly higher whereas the Bax and caspase 3 expression levels were significantly lower in ischemic postconditioning group and fasudil hydrochloride group than in I/R group（P^0.05）. The Bcl-2 expression level was significantly lower whereas the Bax and caspase 3 expression levels were significantly higher in fasudil hydrochloride＋ LY294002 group than in fasudil hydrochloride group （P%0.05）. The Akt expression level was significantly higher in fasudil hydrochloride group than in I/R group and fasudil hydrochloride＋LY294002 group（P%0.05）. Conclusion Fasudil hydrochloride postconditioning can protect rats against myocardial I/R injury possibly by activating the PI3K-Akt pathway.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2013年第4期416-418,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
蚌埠医学院自然科学基金(Byky1298NF)
