CAJ | 학술논문

目的观察痰瘀同治方对高脂大鼠心肌缺血再灌注损伤(myocardial ischemic-reperfusion injury,MI/RI)Rho/Rho激酶信号转导通路的影响.方法采用随机数字表法将60只SD雄性大鼠随机分为假手术组、模型组、西药对照组及痰瘀同治方高、低剂量组.可逆性冠脉左前降支结扎缺血30 min 再灌注2h复制MI/RI模型,应用RT-PCR及Western blotting法检测各组大鼠心肌RhoA、ROCK Ⅱ mRNA 表达及ROCK下游底物肌球蛋白轻链(MLC)磷酸化水平.结果与模型组比较,痰瘀同治方低剂量组可降低心肌RhoA、ROCKⅡmRNA及磷酸化MLC (p-MLC)水平(P值分别为0.045、0.042、0.023,P均＜ 0.05).结论痰瘀同治方可通过抑制RhoA、ROCKⅡ激活及p-MLC蛋白过度表达而调控Rho/Rho激酶信号转导通路,发挥其对缺血再灌注损伤心肌的保护作用.
목적 관찰담어동치방대고지대서심기결혈재관주손상(myocardial ischemic-reperfusion injury,MI/RI)Rho/Rho격매신호전도통로적영향.방법 채용수궤수자표법장60지SD웅성대서수궤분위가수술조、모형조、서약대조조급담어동치방고、저제량조.가역성관맥좌전강지결찰결혈30 min 재관주2h복제MI/RI모형,응용RT-PCR급Western blotting법검측각조대서심기RhoA、ROCK Ⅱ mRNA 표체급ROCK하유저물기구단백경련(MLC)린산화수평.결과 여모형조비교,담어동치방저제량조가강저심기RhoA、ROCKⅡmRNA급린산화MLC (p-MLC)수평(P치분별위0.045、0.042、0.023,P균＜ 0.05).결론 담어동치방가통과억제RhoA、ROCKⅡ격활급p-MLC단백과도표체이조공Rho/Rho격매신호전도통로,발휘기대결혈재관주손상심기적보호작용.
Objective To investigate the influence of Tanyu-Tongzhi (TYTZ)recipe on Rho/Rho kinase signal transduction pathway of myocardial ischemia-reperfusion injury in high fat-fed rats.Methods 60 SD rats were divided into 5 groups randomly,a sham-operated group,a model group,a western medicine control group,a high-dose group and a low-dose group of TYTZ recipe.The model of ischemia reperfusion of the myocardium was reproduced by ligation of left descending artery for 30 min followed by releasing the ligation for 2 hours in rats.The downstream substrates of ROCK myosin light chain (MLC) phosphorylation expression of myocardial tissues in rats were detected by Western blotting method.The levels of RhoA,ROCK Ⅱ mRNA were determined with RT-PCR.Results Compared with the model group,the expression of p-MLC and RhoA,ROCK Ⅱ mRNA were lower in low-dose group of TYTZ,there were significant differences between the two groups(P=0.004、0.003、0.018、0.004,P＜0.01).Conclusion The TYTZ Recipe can protect myocardium from MI/RI.The mechanism of action was related to its inhibiting the protein expression of RhoA,ROCK Ⅱ and p-MLC,restraining the activation of Rho/Rho kinase signal transduction pathway.