| BackgroundMyocardial infarction(MI) is a serious hazard cardiovascular disease to human health, which is also one of the main disease of human death and disability worldwide. Consequently, it is vitally important to make clear and unequivocal the risk factors and the pathogenesis of MI for futher prophylaxis and treatment of cardiovascular disease.Recently, an association between environmental factors and MI has been established in many studies, especially the role of fine particulate matter(PM2.5,≤2.5μm aerodynamic diameter) in the atmosphere are brought into a sharp focus. PM2.5 has a small particle size, complex composition, which can enter the body through the respiratory tract plays a role of "toxicity" by its physicochemical properties. Numerous studies show that PM2.5 can significant increase the risk of MI:Mortality was higher among patients of acute coronary syndrome (ACS) who are excessive exposed to higher concentrations of PM2.5; Long-term exposure to fine particulate air pollution is associated with the incidence of cardiovascular disease and death among postmenopausal women. Effect of PM2.5 on MI is vitally associated with not only the concentration grading but the exposure duration. In contrast to the direct effect of short-term exposure, long-term exposure has a bigger and more durable toxicity effects.It is essential for eukaryotic cells to conserve the integrity of their plasma membrane to maintain cellular homeostasis, cell membrane repair mechanism is particularly important in response to various sources of physical, chemical and metabolic factors damage. Studies have shown that PM2.5 can cause cell membrane injury by oxidative stress, Current research also find that myocardial can synthesis and release MG53(Mitsugumin53) which is membrane repair protective protein, overexpression of MG53 can alleviate the membrane damage caused by oxidative stress and effectively inhibit cardiomyocyte death.MG53 is a cardiac and skeletal muscle-specific protein, which plays an essential role in protection of cell membrane against various types of injury. While the plasma membrane emergency damaged, native MG53 can be tightly combined with intracellular vesicle and sarcolemma, then translocated from cytoplasm and fused with plasma membrane in a Ca2+ dependent manner to reseal the coloboma, reduce the necrosis, apoptosis and tissue damage. Moreover, it is considered that activation of MG53 based therapy emerges as a new strategy for acute myocardial infarction.In summary, Speculation has been proposed and proved by MI and PM2.5 exposed model (PM2.5 suspension was administered by intratracheal instillation):PM2.5 significantly exacerbates the degree of MI, which might be due to inhibiting the expression of MG53 in injuerd cardiac muscle.PurposeTo determine the effect of fine particulate matter(PM2.5) on myocardial infarction (MI) and the expression of MG53(Mitsugumin 53) protein in cardiac tissue.Method1. SD rats were subjected to intratracheal instillation PM2.5 for 4 weeks, HE staining was used to test the pathological changes in lung tissue to ensure the model was successful.2. The rats were subjected to ligate the left anterior descending coronary artery to establish the MI model.3. The model of MI first, then PM2.5 intervention. To observe whether PM2.5 reduce the indicators of cardiac function and survival rate, which were observed and detected at 1,2,4 weeks period respectively. Another model is exchange the intervention sequence. Testing the biomarkers in blood serum of MI, to estimate whether the degree is more serious while MI occurs after PM2.5 exposed. In the end, to verify the effect of PM2.5 on MI, TTC staining was used to detect the MI size in both intervention models.4. Immunoblotting was used to detect the protein expression of MG53 in cardiac tissue.Result1.4 weeks after PM2.5 instillation, the pathological of lung tissue slice showed particle deposition by HE staining, which indicates the instillation model succeed.2. Compared with control, rats intervened by PM2.5 had worse cardiac function, reduced survival rate, larger infarct size, and higher MI blood indicators.3. PM2.5 can obviously inhibits the protein expression of MG53 from the injured cardiac tissue.ConclusionNot only did PM2.5 significantly enhances the degree of MI, but decreases the expres-sion of MG53 protein from the injured myocardial tissue. |
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