Effects Of Thymosin Beta 4 On Oxygen-Glucose Deprivation And Reoxygenation-Induced Injury

Cerebral ischemia causes severe brain injury and results in selective neuronal death through programmed cell death mechanisms, including apoptosis and autophagy. Minimizing neuronal injury has been considered a hot topic among clinicians. The present study elucidated the effect of thymosin beta 4 (T beta 4) on neuronal death induced by cerebral ischemia/reperfusion in PC12 cells that were subjected to oxygen-glucose deprivation and reoxygenation (OGD/R). The survival, apoptotic and autophagy rates of PC12 cells were investigated. T beta 4 pre-conditioning prior to OGD/R was performed to evaluate PC12-cell viability and the protective mechanisms of T beta 4. T beta 4 significantly increased cell survival after OGD/R. T beta 4 inhibited the release of lactate dehydrogenase, downregulated malondialdehyde and upregulated the activities of glutathione peroxidase and superoxide dismutase. In addition, T beta 4 attenuated OGD/R-associated decreases in the expression of P62 and the anti-apoptotic protein B-cell lymphoma-2, as well as the upregulation of autophagy mediators, including autophagy-related protein-5 and the ratio of microtubule-associated protein 1 light chain 3 (LC3) II vs. LC3 I. These results suggested that T beta 4 effectively inhibits cell apoptosis and autophagy induced by OGD/R. To the best of our knowledge, the present study was the first to report on the antioxidant, anti-apoptotic and anti-autophagic effects of T beta 4 in neuronal-like PC12 cells. These results suggested that T beta 4 may be explored as a potential treatment for cerebral ischemia.