运动训练调控S1P介导的iNKT淋巴细胞迁移在缺血性脑卒中后炎症反应中的作用和机制研究

Immune inflammation is a major factor in intractable ischemic stroke. Sphingosine 1-phosphate (S1P), as a metabolite of damaged cells, may play a role in the migration of iNKT lymphocytes to the central nervous system and aggravate the inflammatory reaction of the brain. The exercise rehabilitation training increases cerebral blood flow perfusion. The scavenging effect of S1P will affect the migration and distribution of iNKT, and this effect would reduce inflammation in the area of brain damage. In order to verify the theory, the experiment will be performed in vitro and in vivo. Whether the increased cerebral blood flow in exercise training can reduce the content of S1P in the infarct area and inhibits the migration of iNKT lymphocytes to the infarct area. Inflammation and apoptosis rate of endothelial cells around the blood vessels will be relieved for the decrease of S1P and iNKT. Whether or not to reduce the S1P caused by cell damage and thus form a closed and benign circulation pattern. The subject is a part of the central immune system, which has not been reported, and will provide a new target for the immunotherapy of ischemic stroke.

免疫炎症是难治进展型缺血性脑卒中发生发展的主要因素，1-磷酸鞘氨醇( S1P)作为细胞受损的代谢产物，在梗死脑区的聚集有可能介导了iNKT淋巴细胞向中枢的迁移并加重了大脑的炎症反应。运动康复训练增加脑血流灌注，对S1P的清除作用将影响iNKT的迁移和分布，从而达到脑保护作用。为验证该理论，本课题通过体内外实验，研究运动训练增加的脑血流灌注是否能够降低梗死灶S1P的含量，从而抑制iNKT淋巴细胞向梗死灶的迁移，神经炎症和血管周围内皮细胞凋亡的缓解，是否降低由细胞损伤产生的S1P，从而形成闭合良性循环模式。该课题将中枢免疫看做全身免疫的一部分，尚未见相关报道，将为缺血性脑卒中的免疫治疗提供新的靶点。

免疫炎症是难治进展型缺血性脑卒中发生发展的主要因素，1-磷酸鞘氨醇( S1P)作为细胞受损的代谢产物，在梗死脑区的聚集有可能介导了iNKT淋巴细胞向中枢的迁移并加重了大脑的炎症反应。本项目研究初步认为，运动康复训练增加脑血流灌注，对S1P的清除作用将影响iNKT的迁移和分布，从而达到脑保护作用。该课题主要研究血管机制，在研究期间，同时发现提出的血管相关理论也为心脑血管疾病等提供了新的机制。