Knockdown of Long Noncoding RNA Abhd11os Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis in Cardiomyocytes.

Long noncoding RNA is one potential target for the treatment of various disorders. Here, we explored the role of Abhd11os in ischemia/reperfusion-induced myocardial injury, and preliminarily explored the regulatory mechanisms. Relative Abhd11os expression level was examined by qRT-PCR. Western blot was done to measure the expression of apoptotic-related proteins. Cell counting kit-8 assay and flow cytometry were performed to detect cell viability and apoptosis, respectively. ELISA assay was used to ensure the levels of lactate dehydrogenase, creatine kinase, and cardiac troponin I in serum. Besides, the infarct sizes were confirmed by 2,3,5-triphenyltetrazolium chloride and Evans blue staining. Apoptotic rate of cardiomyocytes in myocardial tissues was evaluated by TUNEL assay. Here, increased Abhd11os expression was found in rat myocardial ischemia/reperfusion injury (MIRI) model and hypoxia/reoxygenation-treated cardiomyocytes. Subsequently, our data in vitro showed that upregulation of Abhd11os inhibited proliferation of cardiomyocytes, but promoted cell apoptosis. In animal experiments, myocardial infarct size in MIRI rats was reduced by Abhd11os knockdown. Moreover, downregulation of Abhd11os inhibited apoptosis of cardiomyocytes. Overall, our results revealed that knockdown of Abhd11os could notably attenuate hypoxia/reoxygenation-induced myocardial injury through suppressing apoptosis of cardiomyocytes. These data suggest that Abhd11os may be a potential target for MIRI therapy.