Dissertation
Dissertation > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Myocardial diseases

The Qili Qiangxin DCM rats with adriamycin-induced cardiac structure and function and molecular mechanism

Author DongHongKe
Tutor LiXinLi
School Nanjing Medical University
Course Internal Medicine
Keywords Dilated cardiomyopathy Qili cardiac Metoprolol BNP TNF-α Sarcoplasmic reticulum Ca2-ATP Enzyme
CLC R542.2
Type Master's thesis
Year 2010
Downloads 28
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Objective To investigate different dose Qili strong heart dilated cardiomyopathy induced by adriamycin rat heart function and serum factor and its mechanisms. Methods SD rats were randomly divided into normal control group and model group. Model 2 weeks 6 intraperitoneal injection of doxorubicin 2.5mg * kg -1 made rats DCM model, divided into groups of cardiomyopathy, metoprolol group, Qili heart high dose group, Qili strong hearts dose group, the Qili cardiac low-dose group. After the four groups were taking metoprolol 10 mg * kg -1 , Qili cardiac capsule the cornstarch high dose 1g crude drug * kg -1 , the middle dose 0.5g crude drug * the kg -1 and a low dose of 0.25g crude drug * kg -1 gavage for 6 weeks. Normal control group and the cardiomyopathy group, the same volume of normal saline 6 weeks. Echocardiography in detecting cardiac function index the ELISA assay serum levels of tumor necrosis factor a (TNF-α) and B-type natriuretic peptide (BNP) content, myocardial tissue hematoxylin (HE) staining pathological tests. Cardiomyopathy group and normal control group of cardiac function was significantly reduced left ventricular end systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) a significant increase (P lt; 0.001 and P lt; 0.05), left ventricular ejection fraction (LVEF) and fractional shortening (FS) was significantly lower (P lt; 0.001), serum BNP and TNF-α levels were also significantly higher than the control group (P lt; 0.001). The metoprolol group cardiomyopathy group, a significant improvement in rats with heart failure LVESD in LVEDD, LVEF and FS (P are lt; 0.05), BNP was significantly lower than the cardiomyopathy group (P lt; 0.05), TNF-α level cardiomyopathy group did not change. The Qili the cardiac high dose group and metoprolol group compared heart function was no statistical difference (P gt; 0.05), BNP and TNF-α were statistically significant (P lt; 0.05 and P lt; 0.001). Qili cardiac group (high, medium, low dose) compared with cardiomyopathy group improve LVESD in LVEDD but no significant difference (P gt; 0.05). The the the Qili cardiac high-dose and middle dose group LVEF, FS and normal control group no difference (P gt; 0.05), cardiomyopathy group significantly improved (P lt; 0.05). The cardiomyopathy in serum TNF-α levels were significantly higher than the group of cardiac Qili (high, medium, low dose) (P are lt; 0.001) and normal control group, TNF-α and Qili cardiac group (high, medium, low dose) showed no significant difference (P gt; 0.05). The the Qili cardiac group (high, medium, low dose) serum BNP concentration and normal control group was significantly higher (P lt; 0.05), the Qili cardiac Group (high, medium, low dose) serum BNP levels than myocardial disease was reduced, but no significant difference (P gt; 0.05). The HE staining discovery: the the cardiomyopathy group myocardial existence myocardial partial necrosis. Metoprolol group myocardial fibers, inflammatory cell infiltration, inflammation around the myocardial fiber arrangement still rules, stripes visible. Basically similar to the the Qili the cardiac high dose group, middle dose and low-dose group, the performance rat myocardial fiber arrangement still rules, stripes visible, the infiltration of inflammatory cells in the myocardial fibers. The the conclusions different doses Qili strong heart can be dilated cardiomyopathy rats LVEF and FS reduce serum inflammatory cytokine TNF-α level, to alleviate inflammatory cell infiltration of the myocardial fibers, no effect on serum BNP levels. The study further found: Qili strong heart improve of DCM rats LVEF and FS effects were dose-dependent effect independent of dose to reduce the level of serum TNF-α. Objective To investigate the the Qili cardiac adriamycin-induced dilated cardiomyopathy myocardial tissue of rats sarcoplasmic reticulum Ca 2 -ATP enzyme in. Methods SD rats were randomly divided into normal control group and model group. The model 2 weeks by intraperitoneal injection of doxorubicin 2.5mg * kg -1 made rat model of dilated cardiomyopathy, were randomly divided into groups of cardiomyopathy, metoprolol group. Qili cardiac group. After were metoprolol 10 mg * kg -1 1g crude drug * of the Qili cardiac capsule cornstarch kg -1 gavage six weeks; normal control group and the the cardiomyopathy group of the same volume of saline gavage for 6 weeks. RT-PCR assay myocardial tissue within the sarcoplasmic reticulum Ca 2 -ATP enzyme (SERCA2a) mRNA concentration and its regulatory protein phospholamban (PLB) mRNA concentration, Western-Blotting measured myocardial organization SERCA2a protein content. Cardiomyopathy rats myocardial tissue SERCA2a mRNA PLB mRNA contents of the normal control group was significantly higher (P lt; 0.001 and P lt; 0.05). Metoprolol group SERCA2a mRNA that PLB mRNA contents of the normal control group increased but no significant difference (P gt; 0.05) than cardiac disease were significantly lower (P lt; 0.05). SERCA2a mRNA in the Qili cardiac group and the normal control group the PLB, mRNA levels were significantly higher (P lt; 0.05 and P lt; 0.001); Cardiomyopathy group comparison, SERCA2a mRNA decreased but no significant difference (P gt ; 0.05), PLB mRNA content higher than the the Cardiomyopathy group (P lt; 0.05); metoprolol group were statistically significant (P lt; 0.05 and P lt; 0.001). Cardiomyopathy rats myocardial tissue SERCA2a protein content and normal control group was significantly higher (P lt; 0.001). The metoprolol group cardiomyopathy slightly lower but no statistical difference (P gt; 0.05), compared with the normal control group was significantly higher (P lt; 0.001). The the Qili cardiac myocardial tissue SERCA2a protein content with the normal control group was significantly higher (P lt; 0.001); cardiomyopathy group and metoprolol group was significantly decreased (P lt; 0.05). Conclusion: doxorubicin can induce DCM rat SERCA2a mRNA increased PLB, mRNA, and SERCA2a protein content, over-expression of SERCA2a can worsen heart failure. Qili strong heart can suppress this expression status and reduce oxygen consumption, protection of damaged myocardium, this may be one of the mechanisms Qili cardiac play to improve the cardiac function of DCM.

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