摘要
目的采用蛋白质学方法研究芪苈强心(QLQX)胶囊对心力衰竭大鼠心肌细胞线粒体蛋白表达情况的影响,并探讨其治疗心力衰竭的机制。方法将心肌梗死心力衰竭大鼠模型分为心衰模型组、QLQX(1.0g/kg.d-1)胶囊组、假手术组。灌胃给药,每天一次,连续4周后,差速离心法提取心肌线粒体,双向电泳法分离差异表达的蛋白,凝胶银染后酶切差异蛋白点进行激光解析电离飞行时间(MALDI-TOF)质谱分析,通过Mascot软件在数据库检索。结果共鉴定出11种差异表达的蛋白质,表达上调的有NADH氧化还原酶、ATP合成酶、苹果酸脱氢酶、长链乙酰辅酶A脱氢酶、缩醛酶、肌酸激酶、58 kDa钙调蛋白;表达下调的蛋白有乳酸脱氢酶B、烯醇酶、αB2Crystallin和热休克蛋白27。结论 QLQX胶囊能够部分纠正衰竭心肌线粒体有关能量代谢、氧化应激相关酶的异常表达,可能是其治疗心力衰竭的机制之一。
Objective To study the effect of Qiliqiangxin (QLQX) capsules on expression of myocardial mitochondrial proteins in rats with heart failure (H F) and to explore the mechanisms of treatment of heart failure by using proteomic approach. Methods Rats with HF induced by myocardial infarction were individed into H F model group, QLQX capsules group (1.0g/kg.d-1), sham-operating group after raising for 4 weeks. Than they were given medicine once a day for consecutive 4 weeks. The myocardial mitochondrial proteins were extracted.The different expressed mitochondrial proteins were separated with dimensional electrophoresis(2DE) and analyzed by matrix assisted laser desorption ionization/time-of-flight mass spectrometty(MAIDI-TOF). Results Identified a total of 11 kinds of differentially expressed proteins.Proteins are upregulated including eoenzyme NADH oxidoreductase, ATP-synthesizing enzyme, malic dehydrogenase, long-chain acetyI-COA dehydrogenase, aldolase, creatine kinasc, 58 kDa calmodulin, Proteins are downregulated including lactate dehydrogenase B, enolase, αB2Crystallin, heat shock protein 27. Conclusion QLQX capsule enables mitochondrial enzyme regulating energy metabolism and oxidative stress expression changes in rats with HF and can partially correct abnormality of energy metabolism and oxidative stress, which may be one mechanism for the treatment of heart failure.
出处
《中国分子心脏病学杂志》
CAS
2014年第3期949-952,共4页
Molecular Cardiology of China
基金
国家自然科学基金(81270235)
陕西省科技攻关基金(2012K15-01-01)