Knockdown of circular RNA circMAT2B reduces oxygen-glucose deprivation-induced inflammatory injury in H9c2 cells through up-regulating miR-133.

Myocardial infarction (MI) is the main cause of morbidity and mortality. Reperfusion ways can cause damage to cardiomyocytes. CircMAT2B, a novel circRNA, takes positive roles in regulating glucose metabolism under hypoxia. Therefore, we aimed to explore the effects of circMAT2B on MI. Oxygen-glucose deprivation (OGD)-induced H9c2 cell model was employed to stimulate MI. Ex-circMAT2B, si-circMAT2B, miR-133 inhibitor and relative control were transfected into H9c2 cells. qRT-PCR was employed to examine levels of circMAT2B and miR-133. Cell activity, apoptosis, ROS generation and release of inflammatory factors were assessed by CCK-8, flow cytometry, ROS species assay kit and ELISA, respectively. Moreover, the expression of apoptosis-related and pathway-related factors was detected through western blot analysis. The results showed that circMAT2B expression was notably up-regulated by OGD treatment. Moreover, circMAT2B knockdown could effectively decrease OGD-induced the increasing of apoptosis, ROS generation and the expression of IL-1β, IL-6 and TNF-α. Besides, miR-133 was positively regulated by si-circMAT2B. CircMAT2B knockdown attenuated OGD-induced H9c2 cell damage and alleviated OGD-induced the inhibition of PI3K/AKT and Raf/MEK/ERK pathways through up-regulating miR-133. In brief, circMAT2B knockdown works as an inflammatory inhibitor in OGD-induced H9c2 cells inflammatory injury through up-regulating miR-133.