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目的探讨visfatin的神经保护作用是否通过对NG2细胞的调节实现。方法采用线栓法制备大脑中动脉阻塞(MCAO)的局灶性脑缺血再灌注模型。选用30只成年雄性WKY大鼠,随机分为假手术(Sham)组、脑缺血模型组、假手术+FK866(visfatin特异性酶抑制剂)治疗组、脑缺血+FK866治疗组。后两组给予FK866 1mg/(kg.d)灌胃,连续14d。治疗7d后分别进行假手术或MCAO手术。手术7d后,用免疫荧光组织化学法检测各组大鼠大脑内NG2阳性细胞数量。结果假手术+FK866组与假手术组相比,大鼠脑内NG2细胞差异无统计学意义;脑缺血模型组与假手术组相比,梗死中心区NG2细胞数减少(P<0.01),半影区NG2细胞数增加(P<0.01),对侧区无变化;脑缺血+FK866治疗组与脑缺血模型组相比,以上各区域NG2细胞数的改变差异无统计学意义。结论抑制visfatin对正常大鼠以及脑缺血再灌注损伤大鼠大脑内NG2细胞数目没有明显的影响,visfatin的神经保护作用可能与NG2细胞无关。
Objective To investigate whether the neuroprotective effect of visfatin is achieved through the regulation of NG2 cells. Methods The focal cerebral ischemia-reperfusion model of middle cerebral artery occlusion (MCAO) was established by thread plug method. Thirty adult male WKY rats were randomly divided into sham group, cerebral ischemia model group, sham operation + FK866 (visfatin specific enzyme inhibitor) treatment group, cerebral ischemia + FK866 treatment group. The latter two groups were given FK866 1mg / (kg.d) gavage for 14 days. After 7 days of treatment, respectively, sham operation or MCAO surgery. Seven days after surgery, the number of NG2 positive cells in the brain of each group was detected by immunofluorescence histochemistry. Results Compared with the sham operation group, the number of NG2 cells in the ischemic model group and the sham operation group were not significantly different (P <0.01) The number of NG2 cells in the penumbra increased (P <0.01), and there was no change in the contralateral area. There was no significant difference in the number of NG2 cells between the ischemic and FK866 groups compared with the model group. Conclusion Inhibition of visfatin has no significant effect on the number of NG2 cells in normal rats and cerebral ischemia-reperfusion injury rats. The neuroprotective effect of visfatin may not be related to NG2 cells.