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ObjectiveThe specific mechanism of microRNA-133a (miR-133a) involved in the pathological process of atherosclerosis (As) remains an open question. This study aims to explore the role of miR-133a in the regulation of endothelial cell apoptosis.MethodsCultured human coronary endothelial cells (HCAECs) were treated with oxidized low density lipoprotein (ox-LDL). The cell viability was detected by MTT assay. The mRNA levels of Bcl-xl and miRNA (miR-133a, etc) were detected by qRT-PCR method. The expression of anti-apoptotic protein Bcl-xl and cleaved-caspase3 was detected by Western blotting, and the apoptosis rate was detected by flow cytometry. The transient transfection technique was used to observe the effect of overexpression and silencing of miR-133a, on the expression of target gene Bcl-xl protein and endothelial cell apoptosis.Results Ox-LDL was observed to decrease the viability of HCAECs cells and induce HCAECs apoptosis; miR-133a increased abnormally in the apoptosis model; after silencing miR-133a, the decrease of Bcl-xl and the increase of apoptosis rate induced by ox-LDL were partially reversed; the overexpression of miR-133a, Bcl-xl decreased and the apoptosis rate increased, and the difference was statistically significant.Conclusion miR-133a might target and regulate the anti-apoptotic protein Bcl-xl, to induce endothelial cell apoptosis and promote the formation of AS.
ABSTRACT
A large number of basic and clinical studies have shown that the Chinese herbs with promoting blood circulation and resolving phlegm effects could prevent and treat myocardial ischemia-reperfusion injury(MIRI) by regulating lipid metabolism. But its mechanism is not yet clear. The studies show that mitochondrial DNA (mtDNA), microRNAs and lipid metabolism participate in the whole process of MIRI and affect the prognosis. mtDNA mutation is the primary factor to cause myocardial ischemia and reperfusion myocardial cell damage. microRNAs aggravate or reduce MIRI injury by down-regulating or up-regulating related genes expression, while miR-33, as a key regulator of cholesterol transport, regulates lipid metabolism through CROT, PGC-1α, AMPK and other genes located in the mitochondria. There are less studies on correlation between miR-33 and mtDNA, microRNAs. Therefore, further studies on the correlation between miR-33 and mtDNA, microRNAs, as well as the discussions on whether the traditional Chinese medicine (TCM) with promoting blood circulation and resolving phlegm effects could target miR-33 to regulate lipid metabolism and inducemt DNA mutations or deletions, would have important significance for the prevention and treatment of MIRI.
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@#ObjectiveTo explore the characteristics of noncompaction ventricular myocardium under ultrasonic cardiography. Methods8 patients, 1 with non-symptom and other 7 with various cardiac dysfunctions and arrhythmias, accepted ultrasonic cardiography. ResultsNumerous ventricular trabeculae and deep intertrabecular recesses, as well as left ventricular dilatations were found under ultrasonic cardiography.ConclusionNoncompaction ventricular myocardium can be diagnosed with ultrasonic cardiography reliablely.
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@#ObjectiveTo explore the effect of the Breviscapine (Bre) on rabbit's cardiac muscles after ischemic preconditioning (IP).MethodsThe myocardial ischemic reperfusion model was made with 32 New Zealand white rabbits by silk thread passed around the left circumflex coronary artery and the apex. Model animals were randomly divided into four groups: myocardial ischemia-reperfusion (I/R) group, Bre+I/R group, IP group and Bre+IP group. The changes of the endothelin (ET), nitrous oxide (NO) and the enzymes of the cardiac muscle were measured, and the areas of myocardium infarction were analyzed.ResultsBre and IP could decrease the content of ET, the enzymes of the cardiac muscle and myocardial infarction area; increase the content of the NO. Bre+IP could strengthen the role of protecting the ischemic myocardial cells.ConclusionThe Bre can protect the ischemic cardiac muscle. The Bre+IP can strengthen the protective effect of the IP.