法舒地尔对新生大鼠缺氧缺血性脑损伤的脑保护作用

Study on the cerebral protection of fasudil for hypoxic-ischemic cerebral damage of neonatal rats

目的:探讨Rho/ROCK抑制剂法舒地尔对新生鼠缺氧缺血性脑损伤(HIBD)的脑保护作用及可能机制。方法:通过7日龄SD新生鼠制作HIBD模型,分别设置对照组、模型组、用药组,通过免疫组化方法与计算机图像分析技术检测不同时间脑组织神经细胞α-SMA、ROCK-2在缺氧缺血新生大鼠脑组织中的表达。结果:与模型组比较,各用药组神经细胞α-SMA和ROCK-2表达降低,差异有统计学意义(P<0.05或P<0.01);各用药组比较,随着给药剂量的增大及给药时间的提前,神经细胞α-SMA和ROCK-2表达均逐渐下降,各组间比较差异有统计学意义(P<0.05或P<0.01)。结论:法舒地尔可以降低HIBD新生鼠模型的脑组织α-SMA和ROCK-2表达,减轻脑组织缺氧缺血性损伤。在新生鼠HIBD的早期(0 h)给予高剂量法舒地尔干预,其脑保护作用最为显著。

Objective To investigate the effect of the cerebral protection and possible mechanism of fasudil for hypoxic-ischemic cerebral damage （HIBD） in neonatal rats. Methods The HBID model was established, then the mice were randomly divided into different groups. The expressions of α-SMA and ROCK-2 were detected in the newborn rats with ischemia. Results Compared with the model group, expressions of oL-SMA, ROCK-2 decreased in each treatment group with significant differences （P 〈 0.05 or P 〈 0.01）. Following with the increases of administration dose and the administration time, expressions of α-SMA, ROCK-2 decreased gradually with significant differences （P 〈 0.05 or P 〈 0.01 ）. Conclusion Fasudil can reduce the expressions of α-SMA, ROCK- 2 in the newborn mice with hypoxic-ischemic brain damage to attenuate the brain tissue hypoxic-ischemic injury. The protective effect on brain is significant by giving high-dose fasudil in the early neonatal rat HIBD （0 h）.