盐酸法舒地尔对NF200在新生大鼠缺氧缺血性脑损伤中表达的影响

目的：利用新生大鼠缺氧缺血性脑损伤（Hypoxic-ischemic brain damage,HIBD）动物模型,检测HIBD脑组织中神经丝蛋白-200 （Neurofilaments Protein-200,NF200）表达的动态变化,观察盐酸法舒地尔（Fasudil Hydrochloride Injection）对大鼠NF200表达的影响及对神经损伤后的保护与修复作用.方法：将新生7d龄Wistar大鼠120只,随机分为假手术组（Sham 组,40只）,缺氧缺血作用（HIBD组,40只）,法舒地尔治疗组40只,每组再分为6h、12h、24h、72h、7d,5个亚组.Sham组只做左颈总动脉分离.HIBD组,法舒地尔组做左侧颈总动脉永久性结扎及缺氧处理后,分别腹腔注射生理盐水和法舒地尔（10mg/kg）.采用免疫组化法检测海马区NF200的表达.结果：Sham组：可见NF200有微量表达,各组间无统计学意义.HIBD组：NF200阳性细胞在造模6h出现表达,12h开始下降,24h降到最低,此后逐渐升高.与Sham组NF200阳性细胞数比较差异有统计学意义（P＜0.01）.法舒地尔治疗组各时间点NF200的表达均高于HIBD组,差异有统计学意义（P＜0.01）.HIBD组和法舒地尔组阳性细胞数明显多于Sham组,差异有统计学意义（P＜0.01）.结论：法舒地尔可能通过抑制Rho/Rock通路促进轴突再生和修复进而使NF200的表达增加.

Fasudil hydrochloride NF200 expression in hypoxic-ischemic brain injury

Objective.Hypoxic- ischemic brain injury HIBD animal models are used to detect the dynamic change of NF200 expression in HIBD brain tissue, and to observe the influences of hydrochloric acid fasudi （Fasudil Hydrochloride Injection） on rats NF200 expression and its effects of protection and repair of nerve in- jury. Method： 120 Seven- day-old Wistar rats were randomly divided into sham operation group （Sham group, 40）,Hypoxia ischemia （ HIBD group, 40）, fasudil treatment group （40）, and each group is divided into 6h, 12h,24h, 72h,and 7d , 5 sub groups in total. Rats in Sham group were only operated separation of the left common carotid artery. Rats in HIBD group and fasudil group were operated permanent left common carotid artery ligation and hypoxia, followed by intraperitoneat injection of saline and Fasudil Seoul 10mg/kg. Immuno- histochemical method to assay the expression of NF200 in hippocampus district. Results：Sham group： visible NF200 trace expression among the groups was not statistically significant. HIBD group ： NF200 -- positive cells in the modeling 6h expression began to decline at the 12h, and reached the minimum at the 24h,then gradually increased. It was statistically significant when the NF200 positive cells were compared with those in Sham group （P 〈 0.01）. NF200 expression of fasudil treatment group at each time point were higher than that in HIBD group, and the difference was statistically significant （P 〈 0.01）. The positive cells in HIBD group and fasudil group were significantly more than that in sham group, and the difference was statistically significant （P 〈 O. 01）. Conclusion： Fasudil may increase NF200 expression through inhibiting Rho/Rock pathway and promoting axonal regeneration and repair.