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Abstract Background Myocardial ischemia reperfusion injury (MIRI) is defined as tissue injury in the pathological process of progressive aggravation in ischemic myocardium after the occurrence of acute coronary artery occlusion. Research has documented the involvement of microRNAs (miRs) in MIRI. However, there is obscure information about the role of miR-130a-5p in MIRI. Herein, this study aims to investigate the effect of miR-130a-5p on MIRI. Methods MIRI mouse models were established. Then, the cardiac function and hemodynamics were detected using ultrasonography and multiconductive physiological recorder. Functional assays in miR-130a-5p were adopted to test the degrees of oxidative stress, mitochondrial functions, inflammation and apoptosis. Hematoxylin and eosin (HE) staining was performed to validate the myocardial injury in mice. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to assess the expression patterns of miR-130a-5p, high mobility group box (HMGB)2 and NF-κB. Then, dual-luciferase reporter gene assay was performed to elucidate the targeting relation between miR-130a-5p and HMGB2. Results Disrupted structural arrangement in MIRI mouse models was evident from HE staining. RT-qPCR revealed that overexpressed miR-130a-5p alleviated MIRI, MIRI-induced oxidative stress and mitochondrial disorder in the mice. Next, the targeting relation between miR-130a-5p and HMGB2 was ascertained. Overexpressed HMGB2 annulled the protective effects of miR-130a-5p in MIRI mice. Additionally, miR-130a-5p targets HMGB2 to downregulate the nuclear factor kappa-B (NF-κB) axis, mitigating the inflammatory injury induced by MIRI. Conclusion Our study demonstrated that miR-130a-5p suppresses MIRI by down-regulating the HMGB2/NF-κB axis. This investigation may provide novel insights for development of MIRI treatments.

Abstract For any positive integer n, let a(n) denotes the square complements of n. That is, a(n) is the smallest positive integer such that na(n) is a perfect square number. [...]

Despite significant medical advances, congestive heart failure remains associated with high mortality rate. Therefore, there is a continuing need for better therapeutics. In this study, we have examined the effect of daidzein against congestive heart failure induced by administration of doxorubicin. Blood pressure, electrocardiogram, B-type natriuretic peptide, and markers of oxidative stress were assessed as measures of cardioprotective effect of daidzein. To further assess the mechanism, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, Western blot assay, and histopathology were performed. Daidzein reduced blood pressure, reversed the altered pattern of electrocardiogram, levels of B-type natriuretic peptide, and oxidative stress markers in doxorubicin-induced cardiotoxicity in rats. Furthermore, treatment with daidzein ameliorated apoptosis and expression of proinflammatory proteins and oxidative pathway [ABSTRACT FROM AUTHOR]