Based on its known ability to inhibit oxidative stress-induced apoptosis in lung, heart, and brain tissue, we investigated the effect of hydrogen on wound tissue apoptosis to identify its potential mechanism of action. The results of this study also supported our hypothesis on the ability of hydrogen to inhibit apoptosis. Expression of Bcl-2protein indicates an anti-apoptotic effect, which can also inhibit autophagy. Combined with the pro-apoptotic protein Bax, the ratio of Bax/Bcl-2 reflects the activation of apoptosis. In addition, burn-induced oxidative stress can prompt phosphorylation of thep38 MAPK Etizolam signal and HJC0350 further activate caspases, ultimately leading to cell apoptosis. The anti oxidant property of hydrogen may influence tissue apoptosis by affecting Bax/Bcl-2 expression and the above-mentioned pathway. Although we observed an elevated level of autophagy in wounds during the early stage after deep burns, as observed in other reports, and applied HS intervention, we still cannot conclude with certainty that autophagy plays a survival or pro death role in wound progression postburn. Generally speaking, autophagy is an in vivo pathway that can degrade cellular macromolecule waste via lysosomes and provide the materials necessary to maintain cellular metabolic turnover and homeostasis.This process has also been reported to play dual roles in cell survival and cell death, and the impairment or activation of autophagy is associated with the development of various diseases. Autophagy serves acytoprotective role against various insults, such as infection, ischaemia, and inflammation, among others. However, autophagy may also mediate programmed cell death when it can not restore tissue cell homeostasis following an in super able stimulus. With regard to burn wound progression, two distinct viewpoints have been offered. Utilising the rat hot-water burn model, Xiao Metal. reported that autophagy plays a role in the pro survival mechanism against ischaemia and inflammation in the deeper dermis during the later stages of burn injury, as a complement to apoptosis.