| Background and purposeAcute myocardial infarction (AMI) can occur when coronary atheroscleroticplaque on the basis of acute thrombotic occlusion caused by coronary artery spasm, afew cases caused by inflammation, thrombosis, malformed occlusion, all those factorscontribute to long term myocardial cell ischemia or even necrosis. Acute myocardialinfarction is a type of coronary heart disease. Restoring blood flow timely andeffectively is an important treatment for AMI. Recently, percutaneous coronaryIntervention (PCI) as the primary treatment have benefit a wide range of clinicalcoronary heart disease patients who suffer from acute myocardial infarction andunstable angina; but some patients who suffer from stable angina and coronary arterydisease are not suitable for non-adaptive surgical treatment, However, life stylechanges and drug therapy become the main therapy for these patients, as well knownthe best drug treatment (OMT). Furthermore, the intervention of proteins or genetherapy result in promoting angiogenesis is becoming increasingly assertive inclinical studies. miRNA is play an important regulating role in respect of cell proliferation,differentiation, apoptosis, and many other biological processes. Recent studiesdiscovered that miRNA is also involved in regulating the developmental processes ofthe cardiovascular system diseases. miRNA plays a necessary part in the repairprocess of neovascularization after myocardial infarction occurs. miR-126is a typeof miRNA which recently found to have a significant role in promoting angiogenesis.Hence,miR-126has become a hot research topic recently. miR-126is located on theexpression of endothelial cell-specific intron egfl7, the transcription together withegfl7by inhibiting the expression of two negative regulator of angiogenesis andSpred-1involved in angiogenesis PI3KR signal transduction, maintaining vascularintegrity, miR-126plays an important function in the process of angiogenesis. Withlipid-lowering statins, anti-inflammatory, antioxidant, protecting endothelial cells topromote angiogenesis, anti-platelet aggregation function has been constantlyconfirmed in clinical studies. The Mechanisms of angiogenesis effects of statinsfamily medications is still in the process of continuing study without a clear definiteexplanation regarding its pharmacodynamics. Therefore, we have established a ratmodel of myocardial infarction, and using rosuvastatin intervention, observed theexpression of miR-126and its effects on microvascular density (MVD), in order tofurther explore their relationship with angiogenesis, to provide new evidence by usingrosuvastatin in acute myocardial infarction after vascular tissue regeneration toprovide a new basis.Material and Methods80healthy clean adult SD rats were purchased from experimental animal center,Zhengzhou University; certificate of conformity is SCXK (Henan):2011-0005. Theyare2to3months old males and females rats, body mass range from225~350g.After acute myocardial infarction model, there are62survivals were randomlydivided into two groups by31in each group. The next day rosuvastatin groupreceived rosuvastatin10mg/(kg d) constantly in six weeks, the model group weregiven the same amount of solubilization solvent gavage for6weeks, of which therewere four in each group died, animals were killed infarcted tissue. Immunohistochemical SP method infarction microvessel density (MVD), the use of expression level of real-time PCR detection of miR-126. Apply to SPSS18.0processing data. Byusing two independent samples test to compare two groups of infarcted tissue MVDand expression of miR-126in rat myocardium, and correlation analysis using twoindicators to discuss the relationship between rosuvastatin and myocardial infarct.Test level=0.05.ResultsImmunohistochemical staining showed that: the rosuvastatin group myocardialinfarction tissue microvessel density (MVD) increased significantly, while higherthan that of model group. There was a statistically significant difference between theresults of the two groups (P <0.05).Real-time PCR results showed: the expression levels of the statin rosuvastatingroup infarcted tissue miR-126was significantly higher than the model group, thedifference was statistically significant (P <0.05).Correlation analysis showed: the rosuvastatin group myocardial infarctionmicrovessel density (MVD) expression levels of miR-126in rats showed a positivecorrelation (r=0.720, P=0.026).Conclusion1Rosuvastatin can promote vascular tissue regeneration after rats attacked withacute myocardical infarction.2Rosuvastatin can unregulate the expression levels of miR-126.3Infarction angiogenesis of Rosuvastatin rats group and their expression levelsof miR-126is positively related to acute infarct myocardial tissue, we hypothesizedthat rosuvastatin promote angiogenesis in infarcted tissue by upregulating theexpression of miR-126. |
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