Background: It is considered that circRNA can participate in regulating the occurrence and effects of ventricular arrhythmia (VA) through competing endogenous RNA (ceRNA) mechanism, regulating pre-mRNA and regulating parental gene expression. Therefore, we used animal modeling and high-throughput differential screening to screen out circRNA related to VA and study its possible mechanism of action on VA.Methods: The rat model of myocardial ischemia VA was established. High-throughput screening of the differentiated circRNA was conducted and verified by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot. Lv-circRNA01724 lentivirus was constructed using molecular biology.Primary isolation of the rat cardiomyocytes, hypoxia modeling, Lv-circRNA01724 transfection, mode of action verification, and dual luciferase detection of circRNA01724 and miR-323-5p was performed.Results: Through qRT-PCR verification of circRNA01724, circRNA02230, circRNA02088, miR-323-5p, miR-330-5p, and miR-324-3p expressions, circRNA01724 was selected as the research object. Detection by Western blot showed significantly lower Cx43, ZO-1, and α-catenin expressions in rat myocardial tissue in the model group compared with the control group at 1, 7, 14, and 28 days old. On identification of the isolated primary rat cardiomyocytes by immunofluorescence, the α-SMA characteristic protein expression indicated that the isolation was successful. Verification of rat cardiomyocytes transfected with Lv-circRNA01724 suggested overexpression in cells. The miR-323-5p was also highly expressed in the rat cardiomyocyte hypoxia model following Lv-circRNA01724 transfection. Detection by flow cytometry showed that modeling of the transfected Lv-circRNA01724 had a significant increased apoptotic rate.Detection by Western blot showed that modeling of the transfected Lv-circRNA01724 cells had significantly decreased Cx43, ZO-1, and α-catenin compared with the model group.Conclusions: High-throughput screening of circRNA01724 can promote the apoptosis of hypoxic cardiomyocytes, which is related to the rat model of myocardial ischemia VA and may be a potential target for the treatment of VA.

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.