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Study The Mechanism On Which Supplementing Qi And Activating Blood Chinese Drugs Protect The Ischemic Myocardium

Posted on:2017-03-07Degree:MasterType:Thesis
Country:ChinaCandidate:H J YanFull Text:PDF
GTID:2334330488970039Subject:Integrative Medicine
Abstract/Summary:PDF Full Text Request
Part 1 The influence of Supplementing qi and activating blood Chinese drugs on the score of blood stasis syndrome and incidence rate of angina pectoris after percutaneous coronary intervention curing acute coronary syndromeObject:To observe the influence of supplementing qi and activating blood Chinese drugs on angina incidence and blood stasis syndrome score of patients who was diagnosed as acute coronary syndrome (ACS) and went through percutaneous coronary intervention (PCI).Methods:93 patients from Xiyuan hospital and Anzhen hospital being diagnosed as ACS, who went through PCI successfully and meeting the inclusion criteria, were randomly divided into control and experimental groups. Two groups of patients were given medical treatment the next day after surgery. Patients in the control group get conventional drugs based guidelines after PCI recommended, patients in the experimental group get supplementing qi and activating blood Chinese drugs as 2 Xin gyue Capsules and 2 Compound Chuan xiong Capsules, three times a day on the basis of recommended western medicine. Record the angina incidence and blood stasis syndrome scores before treatment and 1 month,3 months and 6 months after treatment to assess the angina incidence and blood stasis syndrome scores before and after the treatment. Then, compare the incidence of angina and the improvement of blood stasis syndrome at 1 month,3 months and 6 months after treatment between two groups to observe if added supplementing qi and activating blood Chinese drugs can further reduce the incidence of angina pectoris and the scores of blood stasis syndrome after PCI in patients with ACS.Results:The basic data analysis of two groups showed that they are comparable(P>0.05). The angina incidence rate and blood stasis syndrome(BSS) scores of two groups were compared before and after treatment, which shows that both groups could reduce angina incidence rate and BSS scores(P<0.01). Compared with control group, experimental group showed a better improvement in blood stasis syndrome after 3 months'treatment (P<0.01); and it showed an obvious decrease in the incidence of angina after 6 months'treatment(P<0.05).Conclusion:Both standard treatment and plusing supplementing qi and activating blood Chinese drugs can significantly reduce angina incidence and BSS scores in patients with ACS(P<0.01). Treated with standard therapy plusing supplementing qi and activating blood Chinese drugs for 3 months can reduce the BSS scores significantly, and it can reduce the incidence of angina significantly after PCI for 6 months'treatment.Part 2 Study the influence of supplementing qi and activating blood Chinese drugs on mitochondrial biogenesis protein in rat myocardium after acute myocardial infarctionObjective:To observe the influence of supplementing qi and activating blood Chinese drugs compatibility Panax quinquefolius saponin (PQS) and refined Xue fu Capsules on AMPK activated-mitochondrial biogenesis protein in rats myocardium after acute myocardial infarction (AMI).Methods:150 clean SD male rats, fed with high-fat diet for 28 d, after anesthetized with 4% chloral hydrate,65 of them were made as AMI model successfully by descending artery ligation. And all of AMI model rats were randomly divided into model group, simvastain group, activating blood group, Supplementing Qi group, supplementing qi and activating blood Chinese drugs group, for 13 rats in each group. And set 13 rats as sham group(only puncture.without ligation). All the rats were gavaged with the corresponding drug since the next day of surgery, at the same time, the rats of model group and sham group are gavaged with equal amount of distilled water. After 28d, the rats were anesthetized to measure left ventricular end-systolic inner diameter (LVDs), left ventricular end-diastolic diameter (LVDd), ejection fraction (EF%) by echocardiography. Then, the abdominal aortic blood was collected for detecting the concentration of cardiac troponin T (cTnT), isoenzyme of creatine kinase (CK-MB) by ELISA method. Then the heart was removed for histopathology testing; the gene and protein of AMP-activated protein kinase a2 (AMPKa2), and Peroxisome proliferator-activated receptor-y co-activatorla(PGCla) were tested.Results:Echocardiography showed, compared with sham group, LVDs and LVDd value in model group significantly increased (P<0.05) and EF (%) values decreased significantly(P<0.05). Compared with the model group, the LVDs and LVDd value in supplementing qi and activating blood Chinese drugs group and supplementing qi group reduced obviously (P<0.05); the LVDs and LVDd value in supplementing qi and activating blood Chinese drugs group decreased than supplementing qi group(P<0.05); the LVDs and LVDd value in simvastain group and activating blood group also reduced than model group(P>0.05), the difference between them is not significant. Compared with the model group, EF (%) values in supplementing qi and activating blood Chinese drugs group and supplementing qi group increased significantly(p<0.05); EF (%) value in supplementing qi and activating blood Chinese drugs group increased than supplementing qi group(P<0.05); EF (%) value in simvastain group and activating blood group also increased than model group(P>0.05), the difference between them is not significant.Serology showed, the CK-MB and CTnT serum concentration of the six groups have been compared, comparison between groups shows P>0.05, with the meaning that the difference among the six group is not significant.Pathology showed, by optical microscope, compared with sham group, cardiomyocyte in model group deranged, interstitial congestion and edema; compared with model group, cardiomyocyte in supplementing qi activating blood Chinese drugs group arranged neatly, without interstitial congestion and edema; cardiomyocyte in simvastain group, activating blood group, Supplementing Qi group arranged neatly and with mild interstitial edema compared with model group.By electron microscope, compared with sham group, myofibrillar deranged in cardiomyocyte of model group, with mitochondrial structure destroyed. Compared with the model group, myofibrillar arranged neatly in the cardiomyocyte of supplementing qi activating blood Chinese drugs group, with more mitochondria and no significant destroyed mitochondria; simvastain group, activating blood group, Supplementing Qi group showed an improvement compared with the model group, but not as good as supplementing qi activating blood Chinese drugs group.RT-PCR showed:compared with sham group, AMPK?2 and PGC1? genes of myocardial tissues in model group down-regulated (P<0.05).Compared with the model group, AMPK?2 and PGC1?genes of myocardial tissues in supplementing qi activating blood Chinese drugs group up-regulated (P<0.05), AMPKa2 and PGC1? gene level in simvastain group, activating blood group, Supplementing Qi group also up-regulated (P>0.05).Western Blot showed:compared with sham group, protein expression of AMPKa2 and PGCla of myocardial tissues in model group down-regulated (P<0.05).Compared with the model group, protein expression of AMPKa2 and PGCla of myocardial tissues in supplementing qi activating blood Chinese drugs group up-regulated (P<0.05); protein expression of AMPKa2 and PGC1?in simvastain group, activating blood group, Supplementing Qi group also up-regulated (P>0.05).Conclusion:Supplementing qi activating blood Chinese drugs can attenuate myocardial ischemia after AMI, inhibit left ventricular remodeling, and improve left ventricular function after AMI. The role of protection may related to the promotion of mitochondrial biogenesis protein (AMPKa2and PGC1?) expression in myocardium after ANI.
Keywords/Search Tags:Supplementing qi activating blood, acute coronary syndrome, model rats with acute myocardial infarction, AMP-activated protein kinase, Peroxisome proliferator-activated receptor-? co-activator 1?
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