Abstract
Our research aims to explore the therapeutic effect of circRNA02318 on MIRI rats and the functional mechanism. The MIRI model was constructed in rats. CircRNA02318 overexpressing adenovirus was injected in situ during MIRI perfusion. H9C2 cells were treated with hypoxia for 6 h and reoxygenation for 3 h. Overexpression of circRNA02318 downregulated Drebrin, Nox1, cleaved caspase-3 and Bax in H/R H9C2 cells and MIRI rat heart tissues, promoted the expression of p-Akt/Akt and Bcl-2, and inhibited the apoptosis of H9C2 cells. The volume of myocardial infarction and the release of LDH and TnI in MIRI rats were suppressed by circRNA02318. The Nox1, cleaved caspase-3 and Bax levels were promoted, the level of p-Akt/Akt and Bcl-2 was repressed, and the apoptosis was facilitated by the Drebrin overexpression. Furthermore, the effect of Drebrin overexpression on H9C2 cells was abolished by circRNA02318. Collectively, circRNA02318 exerted therapeutic effects on MIRI rats by inhibiting Drebrin.
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