脑是人体对缺氧最为敏感的器官，脑组织缺血将会导致局部脑组织及其功能的损害，遭受一定时间缺血的组织细胞恢复血流（再灌注）后也可造成脑功能严重受损,而组织损伤程度迅速剧增的情况称缺血再灌注损伤。近年来，关于脑缺血再灌注损伤与血脑屏障破坏的研究已成为一个重要内容。
一项关于“Rho kinase: a new target for treatment of cerebral ischemia/reperfusion injury”的研究表明，盐酸法舒地尔可明显促进脑缺血再灌注后神经功能恢复，改善血脑屏障功能，明显抑制RhoA蛋白表达，上调生长相关蛋白-43和Claudin-5蛋白表达。作者认为，针对Rho激酶进行干预可能是脑缺血再灌注治疗的一个新靶点。此项研究发表在2013年5月第13期的《中国神经再生研究（英文版）》杂志中。（生物谷 Bioon.com）
生物谷推荐的英文摘要
Neural Regeneration Research DOI：10.3969/j.issn.1673-5374.2013.13.003
Rho kinase A new target for treatment of cerebral ischemia/reperfusion injury
Qinghong Cui, Yongbo Zhang, Hui Chen, Jimei Li
Rho kinase inhibitor fasudil hydrochloride has been shown to reduce cerebral vasospasm, to inhibit inflammation and apoptosis and to promote the recovery of neurological function. However, the effect of fasudil hydrochloride on claudin-5 protein expression has not been reported after cerebral ischemia/reperfusion. Therefore, this study sought to explore the effects of fasudil hydrochloride on blood-brain barrier permeability, growth-associated protein-43 and claudin-5 protein expression, and to further understand the neuroprotective effect of fasudil hydrochloride. A focal cerebral ischemia/reperfusion model was established using the intraluminal suture technique. Fasudil hydrochloride (15 mg/kg) was intraperitoneally injected once a day. Neurological deficit was evaluated using Longa’s method. Changes in permeability of blood-brain barrier were measured using Evans blue. Changes in RhoA, growth-associated protein-43 and claudin-5 protein expression were detected using immunohistochemistry and western blotting. Results revealed that fasudil hydrochloride noticeably contributed to the recovery of neurological function, improved the function of blood-brain barrier, inhibited RhoA protein expression, and upregulated growth-associated protein-43 and claudin-5 protein expression following cerebral ischemia/reperfusion. Results indicated that Rho kinase exhibits a certain effect on neurovascular damage following cerebral ischemia/reperfusion. Intervention targeted Rho kinase might be a new therapeutic target in the treatment of cerebral ischemia/reperfusion.
