CircOGDH promotes oxygen-glucose deprivation/reoxygenation-induced neuron injury by targeting the miR-195-5p/brain-specific angiogenesis inhibitor 1-associated protein 2 axis.

Stroke remains a major cause of disability and death worldwide, with inflammation and oxidative stress that play important roles in its pathogenesis. This study aimed to explore the role of circOGDH in stroke and its mechanism of action. SH-SY5Y cells were transfected with circOGDH, miR-195-5p, and brain-specific angiogenesis inhibitor 1-associated protein 2 (BAP2) vectors, and oxygen-glucose deprivation/reoxygenation (OGD/R) models were established. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to assess cell proliferation and flow cytometry was used to measure reactive oxygen species (ROS) activity and apoptotic rates. Inflammatory factor ELISAs were performed. Superoxide dismutase activity and malondialdehyde concentration were measured using assay kits. Luciferase reporters were used to analyze molecular binding. CircOGDH or BAP2 knockdown or miR-195-5p overexpression inhibited the effects of OGD/R on SH-SY5Y cells, including decreased proliferation and superoxide dismutase activity, as well as increased apoptosis, ROS production, malondialdehyde concentration, and inflammatory factor levels. In SH-SY5Y cells, circOGDH targeted miR-195-5p to upregulate BAP2 expression. miR-195-5p inhibition or BAP2 overexpression eliminated circOGDH knockdown-elicited protection of SH-SY5Y cells against OGD/R. CircOGDH aggravates OGD/R-caused SH-SY5Y cell injury and promotes inflammatory factor secretion and oxidative stress by targeting miR-195-5p to upregulate BAP2 expression.