益气活血复方对慢性心衰大鼠Na~+-K~+-ATP酶、Ca~(2+)-ATP酶及线粒体蛋白的影响
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摘要
目的研究益气活血复方对慢性心衰大鼠心肌Na~+-K~+-ATP酶、Ca~(2+)-ATP酶及线粒体蛋白的影响。方法 SD大鼠随机选取10只为正常对照组,其余大鼠以结扎冠脉前降支联合力竭式游泳及饥饿等手段造成慢性心衰模型。将造模成功大鼠随机分为模型组,曲美他嗪组,益气活血复方低、中、高剂量组,每组10只。各组相应予以生理盐水,曲美他嗪和益气活血复方低、中、高剂量连续灌胃7周后,取心肌组织和血清。利用线粒体分离方法测定Na~+-K~+-ATP酶和Ca~(2+)-ATP酶及线粒体蛋白的表达。结果与正常对照组比较,模型组心肌Ca~(2+)-ATP酶、Na~+-K~+-ATP酶活性和线粒体蛋白浓度显著降低(P<0.05);与模型组比较,曲美他嗪组、益气活血复方组Ca~(2+)-ATP酶、Na~+-K~+-ATP酶活性及线粒体蛋白浓度显著上升(P<0.05)。结论益气活血复方可能通过促进心肌细胞Na~+-K~+-ATP酶、Ca~(2+)-ATP酶活性的增强和提高线粒体蛋白浓度,参与调节心肌细胞的能量代谢过程,来发挥其治疗心力衰竭的作用。
Objective To investigate the effect of compound Yiqi Huoxue prescription on Na~+-K~+-ATPase, Ca2 +-ATPase,and mitochondrial protein in the myocardium of rats with chronic heart failure. Methods Ten Sprague-Dawley rats were randomly selected as normal control group. A rat model of chronic heart failure was established by ligation of the anterior descending branch of the coronary artery combined with exhaustive swimming and hunger. After modeling, the rats were divided into model group,trimetazidine group, and low-, middle-, and high-dose compound Yiqi Huoxue prescription groups, with 10 rats in each group.These groups were treated by normal saline, trimetazidine, and low-, middle-, and high-dose compound Yiqi Huoxue prescription,respectively, by gavage for 7 consecutive weeks, and then the myocardial tissue and serum were harvested. The mitochondrial separation method was used to measure the expression of Na~+-K~+-ATPase, Ca2 +-ATPase, and mitochondrial protein. Results Compared with the normal control group, the model group had significant reductions in the concentrations of Ca~(2+)-ATPase, Na~+-K~+-ATPase, and mitochondrial protein in the myocardium(P <0.05); compared with the model group, the trimetazidine group and low-, middle-, and high-dose compound Yiqi Huoxue prescription groups had significant increases in the concentrations of Ca~(2+)-ATPase, Na~+-K~+-ATPase, and mitochondrial protein in the myocardium(P<0.05). Conclusion Compound Yiqi Huoxue prescription plays an important role in the treatment of heart failure by promoting the activities of Na~+-K~+-ATPase and Ca~(2+)-ATPase, increasing the concentration of mitochondrial protein, and participating in the regulation of energy metabolism of cardiomyocytes.
Objective To investigate the effect of compound Yiqi Huoxue prescription on Na~+-K~+-ATPase, Ca2 +-ATPase,and mitochondrial protein in the myocardium of rats with chronic heart failure. Methods Ten Sprague-Dawley rats were randomly selected as normal control group. A rat model of chronic heart failure was established by ligation of the anterior descending branch of the coronary artery combined with exhaustive swimming and hunger. After modeling, the rats were divided into model group,trimetazidine group, and low-, middle-, and high-dose compound Yiqi Huoxue prescription groups, with 10 rats in each group.These groups were treated by normal saline, trimetazidine, and low-, middle-, and high-dose compound Yiqi Huoxue prescription,respectively, by gavage for 7 consecutive weeks, and then the myocardial tissue and serum were harvested. The mitochondrial separation method was used to measure the expression of Na~+-K~+-ATPase, Ca2 +-ATPase, and mitochondrial protein. Results Compared with the normal control group, the model group had significant reductions in the concentrations of Ca~(2+)-ATPase, Na~+-K~+-ATPase, and mitochondrial protein in the myocardium(P <0.05); compared with the model group, the trimetazidine group and low-, middle-, and high-dose compound Yiqi Huoxue prescription groups had significant increases in the concentrations of Ca~(2+)-ATPase, Na~+-K~+-ATPase, and mitochondrial protein in the myocardium(P<0.05). Conclusion Compound Yiqi Huoxue prescription plays an important role in the treatment of heart failure by promoting the activities of Na~+-K~+-ATPase and Ca~(2+)-ATPase, increasing the concentration of mitochondrial protein, and participating in the regulation of energy metabolism of cardiomyocytes.
引文
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[11]丁芳萍.丹参注射液对冠心病心绞痛患者心肌能量代谢的影响[J].临床合理用药杂志,2015,8(1):120-121.
[12]林永哲,金鸣,臧宝霞,等.红花黄色素改善大鼠缺氧心肌能量代谢的研究[J].中草药,2003,34(5):436-439.
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[14] TAEGTMEYERH. Energy metabolism of the heart:from basic concepts to clinical applications applications[J]. Currprobl Cardiol,994,19(2):61-86.
[15] NEUBAUERS. The failing heart-an engine out of fuel[J].New England Journal of Medicine, 2007,356(11):1140-1151.
[16] MAACK C, O’ROURKEB. Excitation-contraction coupling and mitochondrial energetics[J]. Basic research in cardiology, 2007,102(5):369-392.
[17] HASENFUSS G, SCHILLINGER W, LEHNARTSE, et al. Relationship between Na+/Ca2+-exchanger protein levels and diastolic function of failing human myocardium[J]. Circulation, 1999,99(5):641-648.
[18] PIACENTINO V. 3rd Cellular basis of abnormal calcium transients of failing human ventricular myocytes[J].Circulation Research,2003,92(6):651-658.
[19]储岳峰,柯永胜,俞国华,等.大鼠心肌缺血再灌注损伤对心肌细胞Na+-K+-ATP酶亚基基因表达的影响与意义[J].中国动脉硬化杂志,2007,15(3):173-176.
[20] SANBE A, TAKEO S, YAMAGUCHI F, et al. Effects of long-term with ACEI inhibitors, captopril, enalapril and trandolapril,on myocardial energy metabolism in rats with heart failure following myocardial infarction[J]. Journal of Molecular and Celluar Cardiology, 1995,27(10):2209-2222.
[2]张艳,杨硕,庞敏,等.益气活血复方对慢性心衰大鼠心肌组织AngII及PKC的影响[J].中华中医药杂志,2008,23(11):999-1001.
[3]宫丽鸿,张艳,高峰.益气活血复方对慢性心力衰竭大鼠心肌组织MMP-1、I型胶原、BNP的影响[J].中西医结合心脑血管病杂志,2011,9(2):189-190.
[4]乔锐,李超,乔峰,等.高剂量曲美他嗪对扩张型心肌病心衰患者预后影响[J].临床军医杂志,2017,5(5):501-503.
[5]魏志静,吉中强.吉中强教授治疗心衰经验[J].湖南中医药大学学报,2016,36(6):68-70.
[6]张艳,礼海,王彩玲.浅谈慢性心衰中医病名病机研究[J].辽宁中医杂志,2011,38(1):12-13.
[7]张艳,宫丽鸿,于睿,等.浅谈慢性心力衰竭中医辨证康复治疗体会[J].天津中医药,2011,28(2)131-132.
[8]唐斌,张金国,谭洪勇,等.黄芪甲苷对慢性心衰大鼠心肌纤维化及能量代谢的影响[J].中国病理生理杂志,2017,33(3):411-416.
[9]张琳,常勃勃,曹婉雯,等.丹参素对大鼠离体心脏缺血再灌注心肌能量代谢的影响[J].中国药科大学学报,2010,41(3):278-282.
[10]黄黎华,陈渊成,程昱,等.丹参水溶性成分含量变化对大鼠离体心肌能量代谢调节的影响[J].中国药科大学学报,2011,42(4):348-353.
[11]丁芳萍.丹参注射液对冠心病心绞痛患者心肌能量代谢的影响[J].临床合理用药杂志,2015,8(1):120-121.
[12]林永哲,金鸣,臧宝霞,等.红花黄色素改善大鼠缺氧心肌能量代谢的研究[J].中草药,2003,34(5):436-439.
[13]刘湘湘,阮君山.太子参多糖对大鼠心肌缺血的保护作用[J].中国民族民间医药,2017,26(17):18-20.
[14] TAEGTMEYERH. Energy metabolism of the heart:from basic concepts to clinical applications applications[J]. Currprobl Cardiol,994,19(2):61-86.
[15] NEUBAUERS. The failing heart-an engine out of fuel[J].New England Journal of Medicine, 2007,356(11):1140-1151.
[16] MAACK C, O’ROURKEB. Excitation-contraction coupling and mitochondrial energetics[J]. Basic research in cardiology, 2007,102(5):369-392.
[17] HASENFUSS G, SCHILLINGER W, LEHNARTSE, et al. Relationship between Na+/Ca2+-exchanger protein levels and diastolic function of failing human myocardium[J]. Circulation, 1999,99(5):641-648.
[18] PIACENTINO V. 3rd Cellular basis of abnormal calcium transients of failing human ventricular myocytes[J].Circulation Research,2003,92(6):651-658.
[19]储岳峰,柯永胜,俞国华,等.大鼠心肌缺血再灌注损伤对心肌细胞Na+-K+-ATP酶亚基基因表达的影响与意义[J].中国动脉硬化杂志,2007,15(3):173-176.
[20] SANBE A, TAKEO S, YAMAGUCHI F, et al. Effects of long-term with ACEI inhibitors, captopril, enalapril and trandolapril,on myocardial energy metabolism in rats with heart failure following myocardial infarction[J]. Journal of Molecular and Celluar Cardiology, 1995,27(10):2209-2222.