| VMC is a direct violation of the virus in the heart of myocarditis caused by transmitted diseases into the main performance, sometimes involving endocardium or pericardium, the pathological features of myocardial cell necrosis and degeneration, and even myocardial fibrosis, cardiac remodeling, and ultimately the development of into dilated cardiomyopathy. Pathogenesis of this disease is not yet entirely clear, both at home and abroad on the pathogenesis of this disease from the molecular virology, molecular immunology, etc. were studied. Tumor necrosis factor (TNF-α)by mononuclear macrophages, and inflammation are the body's immune system play an important regulatory factors, it can directly undermine the myocardial cells, resulting in interleukin abnormal, so that the immune regulatory network dysfunction, myocardial cells and vascular endothelial cell adhesion molecule expression in the immune increase,and promote substantial lymphocyte infiltration of the myocardial cells. Adiponectin is a protein secreted by adipose tissue, the present study suggests that with a wide variety of cardiovascular diseases. Coronary heart disease, heart failure and hypertension plasma adiponectin levels were low fat, and studies have shown that the plasma was low-fat joint occurs when levels of cardiovascular disease risk. Kenei and others studies show that Wulong Tea can increase coronary heart disease in patients with plasma adiponectin levels.β-adrenergic receptor agonists, adenylate cyclase agonists and glucocorticoids can be reduced the expression of adiponectin gene ,butβ-blockers, ACEI and ARB drugs could increase the plasma adiponectin levels.Ouchi found that human aortic endothelial cells by adiponectin after treatment can inhibit TNF-α-induced monocyte adhesion and adhesion molecule expression. Ouchi and Kihara,s study found that adiponectin through the activation of cyclic adenosine monophosphate (cAMP) protein kinase A (PKA) signaling pathway can inhibition of nuclear factor-kB activation and suppress TNF-αinduced nuclear factor-kB inhibitor of cytosolic phosphorylation, and thus to control the inflammatory response of endothelial cells. Physiological concentrations of adiponectin can reduce macrophage secretion of TNF-αand IL-6, and dose-dependent manner to inhibit TNF-αinduced intracellular adhesion molecule-1, E-selectin and vascular cell adhesion molecule-1 in Human aortic endothelial cell surface expression. Recent studies have shown that adiponectin can activate AMPK signaling inhibited myocardial ischemia - reperfusion injury in cardiomyocyte apoptosis, and pass COX2-PGE2 pathway inhibitor in ischemic myocardium of the secretion of TNF-a levels and reduce the extent of viral myocarditis patients, Endothelin -1 inhibition after myocardial infarction related cardiac hypertrophy. Viral myocarditis is to develop the most serious consequences as dilated cardiomyopathy, Liu and others to the pathogenesis of VMC into viral replication period, period of its own immune response in patients with dilated cardiomyopathy and three phase. When the virus will trigger a violation of myocardial a series of immune responses, while the release of a large number of inflammatory cytokines such as IL-1, 2,6,12, tumor necrosis factor, interferon, etc., to stimulate the myocardium, myocarditis caused by disease. At this point will cause the heart energy metabolism. Inflammatory stimulation of energy metabolism at the same time together with the obstacles, lead to cardiac overload, cardiac function and the onset heart failure, the load process of a long time also led to cardiac hypertrophy, cardiac remodeling and expansion into the development of cardiomyopathy. Prompted the current study of adiponectin through its receptor may activate peroxisome proliferator-activated receptor (PPARα) and AMPK signal transduction pathway of two of its physiological role.These two signaling pathway itself with heart inflammation and cardiac hypertrophy, myocardial fibrosis and other closely related. Adiponectin has anti-inflammatory and the impact of the dual role of myocardial remodeling, and the physical conditions and metabolic effects of myocardial development. Therefore, adiponectin further defined itself and its signal transduction pathway and the relationship between viral myocardial contribute to the treatment of viral myocarditis to provide a new target.Selection of the experimental mice infected with CVB3 as a pathogen, the success of the established model of viral myocarditis. The establishment of the control group, virus group and treatment group, drug use and effect of valsartan on CVB3 infected mice by treatment. CVB3 infection in 7,14,21 days after admission with myocardial tissue detected by immunohistochemistry myocardial cells adiponectin and peroxisome proliferator-activated receptor content, while serum adiponectin and tumor necrosis factor -αcontent.Histopathologic examination of myocardial line check, the calculation points of myocardial pathology, statistics of the observed relationship between volume to explore the viral myocarditis in mice the expression of adiponectin and its expression of valsartan, for research on the pathogenesis of VMC progress and treatment to provide a new theoretical basis and experimental evidence.Results: 1. Successfully established a mouse model of viral myocarditis; 2. Viral myocarditis myocardial histopathological changes in mice clearly shows that a large number of myocardial necrosis and inflammatory cell infiltration, and some faults appear and myocardial fibrosis, virus inoculation the first 7 days after the most obvious cardiomyopathy, a gradual reduction of inflammatory cells, only 21 days to see a small number of inflammatory cells, but myocardial fibrosis can be seen by valsartan treatment improved the above-mentioned diseases trends; 3. Compared with the control and treatment group comparison, the virus of mice the level of serum adiponectin minimum, while the highest levels of TNF-α. 4. Compared with the control and treatment group, compared to treatment group, myocardial highest adiponectin, viruses, and the treatment group and myocardial adiponectin were negatively correlated with pathological points, statistically significant difference. 5. Cardiomyopathy in three groups of mice and PPAR adiponectin was positively correlated, statistically significant difference. Conclusion: 1.VMC when serum adiponectin levels were low-fat for serological detection of VMC to provide a reference.2.VMC adiponectin inhibited the expression of TNF-αto reduce the infiltration of cells in myocarditis patients.3. Valsartan increase in myocardial expression of adiponectin to reduce the disease myocarditis lesions.4. PPARαmay be one of the signal transduction pathway of adiponectin . |
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