Hydrogen improves cell viability partly through inhibition of autophagy and activation of PI3K/Akt/GSK3 beta signal pathway in a microvascular endothelial cell model of traumatic brain injury

摘要

Objective:Traumatic brain injury (TBI) is one of the most serious public health problems in the world. Hydrogen (H-2), a flammable, colorless, and odorless gas, has been observed to have preventive and therapeutic effects on brain trauma and other neurological disorders, but its exact mechanism has not been fully clarified. Methods: To further study the mechanism underlying the role of hydrogen gas in alleviating BBB damage after TBI, we performed the scratch injury model on cultured brain microvascular endothelial cells (bEnd.3), which formed the microvascular endothelial barrier - an integral part of the highly specialized BBB. Results: In the case of TBI, hydrogen was able to improve the decline of cell viability induced by TBI. More importantly, inhibition of PI3 K/Akt/GSK3 beta signal pathway or activation of autophagy reduced the protective effect of hydrogen on cell viability, indicating that such protective effect was regulated by PI3 K/Akt/GSK3 beta signal pathway and was related to the inhibition of autophagy. Conclusion: So we concluded that hydrogen improved the cell viability in a microvascular endothelial cell model of TBI partly through inhibition of autophagy, and inhibitory effect of hydrogen on autophagy was exerted by activating PI3 K/Akt/GSK3 beta signal pathway. These findings enriched our knowledge about the mechanism of hydrogen therapy against TBI.