Abstract

Circular RNA (circRNA) is identified as a potential regulator of ischemic stroke (IS) progression. Through GEO database screening, it was found that circ_0059662 was highly expressed in acute IS patients. However, whether circ_0059662 participated in the IS process has not been studied. Oxygen-glucose deprivation/reoxygenation (OGD/R)-induced SK-N-SH cells were established to mimic IS cell models. The expression of circ_0059662, miR-579-3p, and ETS proto-oncogene 1 (ETS1) was measured via quantitative real-time PCR. Cell counting kit 8 assay, EdU assay and flow cytometry were utilized to detect cell proliferation and apoptosis. Western blot was employed to measure protein expression. ELISA was used to detect the levels of inflammation factors, and oxidative stress was determined by assessing SOD activity and MDA level. The relationship between miR-579-3p and circ_0059662 or ETS1 was examined via dual-luciferase reporter assay, RNA pull-down assay and RIP assay. Circ_0059662 was a circular RNA with highly expression in OGD/R-induced SK-N-SH cells. In OGD/R-induced cell injury, circ_0059662 knockdown promoted cell proliferation, and inhibited cell apoptosis, inflammation and oxidative stress. Circ_0059662 served as miR-579-3p sponge to positively regulate ETS1 expression. MiR-579-3p inhibitor and ETS1 overexpression could reverse the inhibition effect of circ_0059662 knockdown on OGD/R-induced cell injury. Besides, MiR-579-3p also could relieve OGD/R-induced SK-N-SH cell apoptosis, inflammation and oxidative stress by targeting ETS1. Our findings indicated that circ_0059662 knockdown alleviated OGD/R-induced SK-N-SH cell injury by sponging miR-579-3p to regulate ETS1 expression.

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