硫化氢对脑外伤后神经元损伤的保护作用及其机制研究

脑外伤是造成青年人神经系统功能障碍的最常见原因，保护神经元成为临床治疗脑外伤的重要措施。硫化氢是近年来发现的气体信号分子家族新成员，在心、脑等多个器官发挥重要的生物学功能。但是，硫化氢在脑外伤中的作用，迄今未见报道。我们首次报道脑外伤后给予外源性硫化氢可减轻脑组织受损程度和神经元受损伤的数量以及改善神经系统功能。但硫化氢在脑外伤后的保护机制仍未阐明。氧自由基是造成神经元损伤发生发展的中心环节。本项目拟在前期研究的基础上，进一步确定外源性硫化氢对脑外伤后神经元的保护作用，通过观察硫化氢对氧自由基产生的影响及可能的作用靶点以及在神经元损伤过程中调控氧自由基产生的信号通路关键分子表达的变化，阐明神经元损伤过程中硫化氢对氧自由基的产生及其诱发凋亡和自噬的调控作用机制，从而为硫化氢作为脑外伤后神经元保护药物用于相关治疗提供理论基础。

Traumatic brain injury (TBI) is the most common cause of young people in the nervous system dysfunction, and to protect neurons become an important measure in the clinical treatment. Hydrogen sulfide (H2S) has been referred to as the third gaseous signaling molecule, which is involved in many physiological functions in mammals, especially in the nervous system and cardiovascular system. However, the role of H2S in TBI has not been reported so far. We found administration of exogenous H2S can reduce brain tissue damage and the number of injured neuron and improve central nervous system function. However, the protective mechanism of H2S after injury has not been elucidated. Oxygen free radicals are the central link of the occurrence and development of neuronal injury. The project intends to further determine on the protective effect of H2S，detect oxidative stress related proteins and clarify the molecular regulation mechanism on the production of oxygen free radicals. This project will play an important role in the comprehensive assessment of pharmacological implications of hydrogen sulfide, and its applications to the field of neuroprotection.