| Congestive heart failure (CHF) has seriously been affected patients' life quality for its high morbidity/mortality. It is difficult to be dealt with clinic approach, because it is unclear pathogenesis. CHF pathogenesis is about a cardiomyopathy of overload caused by abnormal gene expression for energy. Left ventricular remodeling is specific pathology change in the CHF.1 Experimental study on the functional genes regulating CHF with heart deficient syndrome To reveal the function genomics related with the structure and function of CHF. The study used the rat model coronary artery ligation and added rising blood pressure drug in later period. After 10,56,84 days, its cardiac function and structure change were observed with method of gene expression microarray, function; morphology, immunohistochemistry, norphometry, bioinformatics analysis, captopril as positive control, and interfered with drug of different dosage prescriptions of Huoxue Yiqi . To research gene sequence-structure-function in model rat of CHF, gene expression regulated about left ventricle remodeling will be revealed. It will be described how the prescriptions treat CHF. ⑴Observing model's changes in cardiac function with impedance, ECT, blood pressure, morphology, immunohistochemistry during three stages, it was confirmed successful. ⑵Evaluating with unified diagnosis the standard about heart deficient and blood stasis syndrome in combination western medicine integrated with TCM. It showed the rat model characterized with palpitation, breath difficulty, inertia, and tongue violet-dim, fat and bigger. Above of all, the model is in CHF with heart deficient syndrome.⑶Extracted total RNA of infarct and no infarct areas in the left ventricle of model and left ventricle of sham during three stages, detected with 9 pieces of rat gene expression microarray (4096 clones). There are more than one thousand gene expression about thirteen kinds of gene include energy metabolism and cytoskeleton. In infarct area, there are 1086 genes in 10 days, 724 genes in 56 days, 372 genes in 84 days. In no infarct area, there are 196 genes in 10 days, 183 genes in 84 days, 97 genes in the 56 days.⑷Clustering analysis with gene microarray software - Genespring, combined bioinformatics:the result showed : ①Gene expression is serious down regulated about receptor, signal transduction. They cause gene downregulation about metabolism genes (energy metabolism), Ion and channel gene, anti-apoptosis gene, and contraction and relax genes, myocardium embryo gene expression. ② Gene expression is unregulated about cell regulation Protein genes (activating interstitial fibrosis gene, such as FN), DNA Synthesis, pleurisies, reorganization genes, protooncogene and repress oncogene, accelerate early apoptosis gene, cyclin. ③ Phosphogly ceromutase gene is the down regulated 10-folds, which take part in signal transduction, oxidative phosphorylation , energy metabolism. ④ FN is the high unregulated 25-folds, which activates interstitial fibrosis. Gene expression regulated disorder causes left ventricle remodeling, include myocardial cell hypertrophy, necrosis or apoptosis, myofibrosis. It leads to cardiac function decrease.2 Interfering study on the functional genes regulating CHF with heart deficient syndromeTo study the function genomics regulating heart deficient syndrome of CHF with interfering factors, Captopril, as positive control, and prescriptions of Huoxue Yiqi has been used to interfer with the function genes in rats CHF with heart deficient syndrome. The research demonstrated that those interfering factors regulate important genes of left ventricle remodeling in the CHF with heart deficient syndrome.⑴The interfering factors affected on the pathological processes of the rats with CHF and heart deficient syndrome: The model rats were treated with prescription different dosage of Huoxue Yiqi and captopril. According to the dosage of activating blooding herbs/total dosage percentage, there are HXYQ (75%...
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