Hydrogen improves cell viability partly through inhibition of autophagy and activation of PI3K/Akt/GSK3β signal pathway in a microvascular endothelial cell model of traumatic brain injury

Yifeng Wang, Lu Wang, Tianpeng Hu, Feng Wang, Zhaoli Han, Zhenyu Yin, Xintong Ge, Keliang Xie, Ping Lei

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DOI: 10.1080/01616412.2020.1747717 DOI is the universal ID for this study.

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Objective:Traumatic brain injury (TBI) is one of the most serious public health problems in the world. Hydrogen (H2), 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/GSK3β 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/GSK3β 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/GSK3β signal pathway. These findings enriched our knowledge about the mechanism of hydrogen therapy against TBI.

Publish Year 2020
Country China
Rank Positive
Journal Neurological Research
Primary Topic Brain
Secondary Topic Traumatic Brain Injury
Model Cell Culture
Tertiary Topic Oxidative Stress
Vehicle Medium (Dissolved)
pH Neutral
Application Culture Media