中文摘要：

目的探讨Rho激酶（Rhokinase，ROCK）抑制剂法舒地尔（fasudil，FAS）在高氧致新生SD大鼠肺纤维化中的作用。方法新生SD大鼠24只按随机数字表法分为空气＋生理盐水（NS）组（正常对照组）、空气＋FAS组、高氧＋NS组和高氧＋FAS组，分别建立动物模型。在实验的第21天分别取各组新生大鼠行肺组织病理学检查，碱水解法测肺组织羟脯氨酸含量，免疫组化法和Westernblot检测肌成纤维细胞表型标志α-平滑肌肌动蛋白（α-smoothmuscleactin，α—SMA）的表达与分布。结果①病理学检查结果显示，高氧＋NS组肺组织结构紊乱，纤维化严重；高氧＋FAS组较高氧＋NS组明显改善。②肺组织羟脯氨酸测定结果显示，空气＋Ns组和空气＋FAS组无明显差异（P〉0．05），高氧＋Ns组与高氧＋FAS组较空气＋NS组明显增加（P〈0．05），高氧＋FAS组较高氧＋NS明显降低（P〈0．05）。③α-SMA免疫组化和Westernblot检测结果均显示，与空气＋NS组相比，高氧＋NS组和高氧＋FAS组α-SMA的表达显著增强（P〈0．05），而高氧＋FAS组较高氧＋NS组明显减弱（P〈0．05）。结论ROCK抑制剂法舒地尔能一定程度改善高氧致新生大鼠肺纤维化，其机制可能是通过抑制肌成纤维细胞的产生从而减轻肺纤维化。

英文摘要：

Objective To investigate the Rho kinase inhibitor fasudil （FAS） in neonatal rats with hyperoxia-induced lung fibrosis. Method According to the random number tables, twenty-four Sprague- Dawley neonatal rats were randomly divided into 4 groups ： air ＋ normal saline （NS） group, air ＋ FAS group, hyperoxia ＋ NS group and hyperoxia ＋ FAS group. After 21 d, the subjects were sacrificed. The changes of lung histomorphology were observed. Hydroxyproline in the lung was detected by sample hydrolysis method. a-smooth muscle aetin （α-SMA） protein expression in the lung was determined by immunohistochemistry assay and Western blotting. Results Pathological examination showed structural disorder and obvious fibrosis in the lung tissues of hyperoxia ＋ NS group and the signs of improvement in the lung tissues of hyperoxia ＋ FAS group at 21 d. The content of hydroxyproline and α-SMA protein expression in lung tissues were both increased markedly at 21 d in the hyperoxia ＋ NS group and hyperoxia ＋ FAS group compared with the air groups, and were significantly lower at 21 d in the hyperoxia ＋ FAS group than in the hyperoxia ＋ NS group. Conclusion Rho kinase inhibitor fasudil has obvious therapeutic effects on hyperoxia-induced lung fibrosis, probably through myofibroblast inhibition.