| Heart failure is a common end-stage performance of a variety of cardiovascular diseases, which is a big threat to human in 21st century. Heart failure is of poor prognosis with the 5-year survival rate similar to malignant tumor. With the continuous progress of thrombolytic drugs and interventional techniques, the mortality of myocardial infarction is declining significantly. However, it is indicated that heart failure will occur in 1/3 patients among 65-84 after they got AMI. Myocardial microvascular disease is being focused in chronic heart failure induced by AMI. Myocardial micro vessels refer to the capillaries and microvasculature between arterioles and venules with under 100 microns in diameter. Myocardial micro vessels are among the most peripheral circulatory system which have a number of functions involving determining myocardium perfusion, affecting coronary flow reserve, regulating contraction and relaxtion of vessels,keeping a stable blood pressure, adjusting the blood coagulation and anticoagulation, participating in blood vessels structure and secreting vascular active substances. The no-flow phenomena after PCI as well as AMI reperfusion injury are closely related to myocardial microvascular diseases.98 cases AMI with blood supply revascularization observed by Ramo showed that 12.5% of them had poor myocardium perfusion with microangiopathy, thus, the incidence of myocardial remodeling and heart failure after AMI was significantly higher than those had a better myocardium perfusion.Qiliqiangxin is a Chinese herbal medicine compound preparation that extracted from 11 herbs including astragalus, ginseng, salvia, monkshood, et al, which is mainly used for the treatment of patients with mild-to-moderate chronic heart failure. Qiliqiangxin is able to improve the symptom and cardiac function of patients with heart failure and enhance the patients quality of life. The result of clinical evidence-based researches on the treatment of chronic heart failure caused high attention both at home and abroad. However, the mechanism is unclear. Heart failure SD rats after AMI were fed with Qiliqiangxin for 6 weeks, and cardiac function was measured through cardiac ultrasound. We aimed to observe the anti-HF effect of Qiliqiangxin. In addition, MMVECs were cultivated in vitro and then stimulated by hypoxia with Qiliqiangxin pretreatment. Some related indicator of angiogenesis, cell apotosis, cell energy metabolism were detected. We therefore hypothesized that Qiliqiangxin can protect against HF through protection of MMVEC.Acute myocardial infarction(AMI)model was conducted by ligating left anterior descending branch in approximately 200g male SD rats. Evaluating cardiac function by cardiac ultrasound, thus selected those with EF<50%. All the experimental rats were ramdomly divided into 6 groups:(1)Sham group (2)HF+NS group (3)HF+captopril group 50mg/kg/d (4)HF+Qiliqiangxin low dose group 0.3g/kg/d (5)HF+Qiliqiangxin middle dose group 0.6g/kg/d (6)HF+Qiliqiangxin high dose group 1.2g/kg/d. Following 6w gavage, cardiac function was detected once again and rats were sacrificed by cervical dislocation.2 weeks old SD rats were selected. Explants cultivation of cardiac tissues was used to obtain the myocardial micro vessel endothelial cells(MMVEC). Selecting the optimal concentration of Qiliqiangxin extract and oxygen deficient generator was used to induce hypoxia. Cells were divided into three groups and incubated with normal medium, hypoxia medium, hypoxia medium+QLQX. Western Blotting, Elisa, scanning electron microscope were adopted to observe the indicators of angiogenesis, apotosis, energy metabolism, et al.The result showed that, in the level of animal, several cardiac function indexes including EF, FS, LVESV, LVEDV were significantly improved in HF+Qiliqiangxin middle dose group and HF+Qiliqiangxin high dose group compared with controlled group. The effect was similar to captopril. In addition, the sizes of heart of rats with Qiliqiangxin gavage were smaller than controlled group. Therefore, it is indicated that Qiliqiangxin can ameliorate the myocardial remodeling and heart failure after AMI. Moreover, cell experiments showed Qiliqiangxin improved the structure form, apoptosis and energy metabolism of MMVEC, indicating that Qiliqiangxin perform a protective effect on MMVEC through different approaches.In conclusion, Qiliqiangxin may ameliorate chronic heart failure partly by protecting MMVEC.Part oneQiliqiangxin improves cardiac function of rats with heart failure after myocardial infarctionObjective:to demonstrate the improvement of Qiliqiangxin on cardiac function of rats with heart failure after myocardial infarction.Methods:Acute myocardial infarction(AMI)model was conducted by ligating left anterior descending branch in approximately 200g male SD rats. Evaluating cardiac function by cardiac ultrasound, and those with EF<50% were selected one week later. All the experimental rats were ramdomly divided into 6 groups:(1)Sham (2)HF+NS(controlled group) (3)HF+captopril 50mg/kg/d (4)HF+Qiliqiangxin low dose group 0.3g/kg/d (5)HF+Qiliqiangxin middle dose group 0.6g/kg/d (6)HF+Qiliqiangxin high dose group 1.2g/kg/d. Following 6w gavage, cardiac function was detected once again and rats were sacrificed by cervical dislocation. Observing the sizes and shapes of hearts.Results:cardiac function indexes including EF, FS, LVESV, LVEDV, were significantly improved in HF+Qiliqiangxin middle dose group and HF+Qiliqiangxin high dose group compared with controlled group. The improvement effect was similar to Captopril. HF+Qiliqiangxin low dose group seemed no obvious change. The heart sizes of HF+Qiliqiangxin low, middle, high dose and Captopril groups were obviously smaller than controlled (P<0.05).Conclusion:Qiliqiangxin can improve cardiac constriction and relaxation of AMI rats, ameliorate myocardial remodeling and inhibit the development of HF.Part twoQiliqiangxin protect hypoxia induced myocardial micro vessel endotheliumObjective:to demonstrate the protective effect of Qiliqiangxin on myocardial micro vessel endothelium.Methods:(1)Explanting cultivation of cardiac tissues was used to obtain the MMVEC of 2 weeks old SD rats.(2)The Qiliqiangxin extract superfines were dissolved with high glucose DMEM. Selecting the optimal concentration of Qiliqiangxin solution with trypanblue.(3)Cells were divided into three groups and incubated with normal medium, hypoxia medium, hypoxia medium+QLQX. Cell supernatants were collected, and nucleus and cytoplasm protein were extracted. (4)Indicators reflecting endothelial function including ET-1, ICAM-1, VEGF were detected by ELISA, form and ultrastructure of different cell groups were observed with scan microscope and HIF-1α、VEGF、GLUT-1、GLUT-4、bax、bcl-2,et al, were determined by Western blotting.Results:(1) High purity of MMVEC was available by explanting cultivation. Flagstone and tube-like structure were visible. (2)Trypanblue showed that the survival rate of MMVEC was highest in the concentration 0.5mg/ml of Qiliqiangxin (p<0.05) (3)ELISA revealed that compared with hypoxia medium, VEGF in hypoxia medium+QLQX was increased, ICAM-1 was decreased and ET-1 was not changed obviously. Scanning microscope showed abnormal changes in cell morphology and a number of apoptotic bodies were found in cytoplasm in hypoxia medium group, while in hypoxia medium+QLQX group, apoptotic bodies were significantly reduced. WB showed expression of HIF-1α、VEGF、GLUT-1、GLUT-4,bcl-2 were increased in QLQX group, and Bax was decreased compared with hypoxia group (p<0.05)Conclusion:Qiliqiangxin can improve the morphology, function, energy metabolism of MMVEC induced by hypoxia and reduce apoptosis. It is indicated that Qiliqiangxin may ameliorate heart failure through protecting myocardial microvascular endothelium. |
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