S-甲基异硫脲对急性缺血性脑卒中的保护作用

Protective effect of SMT on acute cerebral infarction

目的研究S-甲基异硫脲(SMT)对急性缺血性脑卒中保护作用。方法复制光化学局灶性脑梗死动物模型,通过免疫荧光双标、激光共焦显微镜观察各组缺血半暗带小胶质细胞(microglia MG)中诱导型一氧化氮合成酶(iNOS)的表达;采用电子自旋共振(electron spin resonance,ESR)技术,通过标准添加法检测脑血栓不同时间点NO的含量;运用TTC染色观察SMT治疗对脑梗死灶体积的影响。结果缺血早期2、6 h,与对照组相比,治疗组半暗带的NO含量无变化,梗死灶体积差异亦无显著性。缺血中后期12、24、48 h,SMT明显抑制半暗带MG中iNOS的表达和NO的产生。TTC染色结果提示,对照组12 h梗死灶体积明显增大,24、48h达到高峰,治疗组12 h、24 h、48 h脑梗死灶体积明显减小。结论SMT通过抑制MG中iNOS的表达,减少NO的产生,对急性缺血性脑卒中产生保护作用。

Aim To explore the protective effect of SMT on acute cerebral infarction. Methods Focal cerebral infarction was induced by photochemistry. The expression of iNOS was detected in microglia by double fluorescent immunohistochemistry and laser scanning confocal microscopy. NO content at post-ischemic time points was determined by electron spin resonance （ESR） technique and standard addition method. TTC stain was used to determine the infarct volume. Results At ischemic early period, compared with control group, NO content was not remarkably different after 2 h,6 h of ischemia in the treatment groups, infarct volumes also were not obviously changed. At ischemia mid and late period 12 h ,24 h ,48 h, the expression of iNOS and NO content was suppressed by SMT treatment in microglia. In TTC stain results, infarct volumes were increased obviously after 12 h, and achieved the peak after 24 h,48 h in control groups, infarct volumes in treatment groups were significantly decreased after 12 h,24 h,48 h. Conclusion SMT may play a protective role in acute cerebral infarction by reducing the expression of iNOS and NO content in microglia.