Visfatin对大鼠脑缺血再灌注损伤后NG2细胞数的影响

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。

Effects of visfatin on NG2 cells following cerebral ischemia/reperfusion injury in rats

Objective To investigate the effect of visfatin on the NG2 cell number in the brain of normal rats and rats with cerebral ischemia/reperfusion (I/R) injury. Methods Transient focal cerebral I/R model was established by middle cerebral artery occlusion (MCAO) and a monofilament suture via intraluminal approach in rats. Thirty adult male Wistar-Kyoto rats were randomly divided into four groups, namely, a sham operation group (Sham), a cerebral I/R model group(MCAO), Sham+FK866(a specific inhibitor of visfatin) group, and cerebral I/R+FK866 group. Animals in the latter two groups were intragastrically given FK866 (1 mg/kg·d]) for a consecutive of 14 days; Sham operation or MCAO was performed at the 7^th day of FK866 treatment. The NG2 cells were observed by immunofluorescence staining in animal brains at the 7^th day after surgery. Results There was no significant difference in NG2 cell numbers between the Sham group and Sham + FK866 group. Cerebral I/R model group had significantly less NG2 cells in the core region of infarction(P<0.01) and significantly more in the penumbra area (P<0.01) compared with the Sham group, with no significant change in the contralateral side. The NG2 cell numbers were not significantly different between the cerebral I/R model group and cerebral I/R + FK866 group in the above mentioned areas. Conclusion Inhibition of visfatin shows no noticeable effect on NG2 cell number in the brains of normal and cerebral I/R rats, indicating that the neuroprotective effect of visfatin is not associated with NG2 cells.