Traumatic brain injury (TBI) is one of the most serious public health problems in the world. TBI causes neurological deficits by triggering secondary injuries. Hydrogen sulfide (H₂S), a gaseous mediator, has been reported to exert neuroprotective effects in central nervous system diseases, such as TBI. However, the molecular mechanisms involved in this effect are still unclear. The present study was designed to explore the ability of NaHS, a H₂S donor, to provide neuroprotection in a mouse model of TBI and to discover the associated molecular mechanisms of these protective effects. Here, we found that administration of NaHS not only maintained the integrity of the blood brain barrier (BBB), protected neurons from apoptosis, and promoted remyelination and axonal reparation but also protected mitochondrial function. In addition, we found that autophagy was inhibited after treatment with NaHS following TBI, an effect that was induced by activation of the PI3K/AKT/mTOR signalling pathway. Our study indicated that H₂S treatment is beneficial for TBI, pointing to H₂S as a potential therapeutic target for treating TBI.

颅脑外伤（TBI）是世界上最严重的公共卫生问题之一。TBI通过引发继发性损伤而导致神经功能缺损。硫化氢（H ₂ S）是一种气态介质，据报道在中枢神经系统疾病（例如TBI）中发挥神经保护作用。但是，这种作用涉及的分子机制仍不清楚。本研究旨在探索NaHS（一种H ₂S供体，用于在TBI小鼠模型中提供神经保护作用，并发现这些保护作用的相关分子机制。在这里，我们发现使用NaHS不仅可以维持血脑屏障（BBB）的完整性，可以保护神经元免受凋亡，并促进髓鞘再生和轴突修复，还可以保护线粒体功能。此外，我们发现在TBI后用NaHS治疗后，自噬被抑制，这是由PI3K / AKT / mTOR信号通路激活引起的。我们的研究表明，H ₂ S治疗对TBI有益，指出H ₂ S是治疗TBI的潜在治疗靶标。