Effects of Fasudil on the expression of Nogo-A and NF200 in neonatal hypoxic-ischemic brain damage rats / 中华实用儿科临床杂志

ABSTRACT

Objective To study the effects of Fasudil on expression of Nogo-A and NF200 in neonatal hypoxic-ischemic brain damage(HIBD) rats.Methods One hundred and twenty 7-day-old Wistar rats were divided into 3 groups with random number tableSham operation group (n =40),HIBD group (n =40) and Fasudil group (n =40).Sham group only separated from the common carotid artery,without ligation,direct suture the incision does not do hypoxia; HIBD group were injected with saline; Fasudil group was injected with fasudil(10 mg/kg).The rats were killed at 6 h,12 h,24 h,72 h,7 d,after administration.The pathological changes were observed by means of HE.The expression of Nogo-A and NF200 was studied with immunohistochemical staining.Results 1.Naked eye observationSham group bilateral symmetrical cerebral hemispheres; HIBD group of brain edema aggravated,the visible hemisphere focal necrosis; fasudil treatment group of edema than HIBD group ease.2.HE stainthe structure and shape of brain in Sham operation group were normal.In HIBD group,the cells became edema,karyopyknosis,lyse,and the inflammatory cells became more.The number of edema cells and karyopyknosis decreased in Fasudil group.3.Immunohistochemical stainthere were less expressions of Nogo-A in Sham operation group.It increased slightly after 12 h in HIBD group but decreased later.The expression of Nogo-A in Fasudil group was less than the other two groups at any time except 6 h (P ＜0.01).There was more expression in HIBD and Fasudil group compared with Sham operation group(P ＜0.01).NF200 was less expression in Sham operation group.NF200 appeared after 6 h and became less after 12 h.The expression of NF200 was at 24 h and later became more.The expression of NF200 in Fasudil group was more with HIBD group at each different time (P ＜ 0.01).The expressions of NF200 in Fasudil and HIBD group were more compared with Sham operation group.Conclusions Fasudil can rehabilitate the damaged axon and promote nerve regeneration through controlling the Rho/Rock and make the expression of NF200 increase.