| 摘要: |
| 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 1 mg/(kg·d)灌胃,连续14 d。治疗7 d后分别进行假手术或MCAO手术。手术7 d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。 |
| 关键词: NG2细胞 visfatin 神经保护 脑缺血 再灌注损伤 |
| DOI：10.3724/SP.J.1008.2011.01161 |
| 投稿时间：2011-04-05修订日期：2011-06-09 |
| 基金项目:国家杰出青年科学基金(30525045), 国家重点基础研究发展计划("973"计划)课题(2009CB521902), 上海市优秀学科带头人计划A类(10XD1405300), 全国优秀博士论文基金(200369), 国家科技重大专项"重大新药创制"(2009ZX09303-002). |
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| Effects of visfatin on NG2 cells following cerebral ischemia/reperfusion injury in rats |
| TIAN Wei-wei,WANG Pei,MIAO Chao-yu* |
(Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China
*Corresponding author.) |
| Abstract: |
| 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 7th day of FK866 treatment. The NG2 cells were observed by immunofluorescence staining in animal brains at the 7th 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. |
| Key words: NG2 cells visfatin neuroprotective brain ischemia reperfusion injury |
