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首页> 外文期刊>Life sciences >Inhibition of Rho kinase by fasudil hydrochloride attenuates lung injury induced by intestinal ischemia and reperfusion.
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Inhibition of Rho kinase by fasudil hydrochloride attenuates lung injury induced by intestinal ischemia and reperfusion.

机译：盐酸法舒地尔对Rho激酶的抑制作用减弱了肠缺血和再灌注引起的肺损伤。

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AIM: The aim of this study is to evaluate the role of Rho-kinase in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R) and the preconditioning effects of fasudil hydrochloride. The novel therapeutic approach of using Rho-kinase inhibitors in the treatment of intestinal I/R is introduced. METHODS: Sprague-Dawley (SD) rats were divided into 4 groups: intestinal I/R group, two fasudil pretreatment groups (7.5 mg/kg and 15 mg/kg), and controls. Intestinal and lung histopathology was evaluated; myeloperoxidase (MPO) and superoxide dismutase (SOD) levels in lung parenchyma were determined. Serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured. eNOS and P-ERM expression were measured by Western Blot. RESULTS: Lung and intestinal injury were induced by intestinal I/R, characterized by histological damage and a significant increase in BALF protein. Compared to controls, serum TNF-alpha, IL-6, and lung MPO activity increased significantly in the I/R group, while SOD activity decreased. A strongly positive P-ERM expression was observed, while eNOS expression was weak. After fasudil administration, injury was ameliorated. Serum TNF-alpha, IL-6, lung MPO and P-ERM expression decreased significantly as compared to the I/R group, while SOD activity and eNOS expression increased significantly. SIGNIFICANCE: Rho-kinase plays a key role in the pathogenesis of lung injury induced by intestinal I/R. The inhibition of the Rho-kinase pathway by fasudil hydrochloride may prevent lung injury.
机译：目的：本研究旨在评估Rho激酶在肠缺血/再灌注（I / R）引起的肺损伤的发病机制中的作用以及盐酸法舒地尔的预处理作用。介绍了使用Rho激酶抑制剂治疗肠道I / R的新方法。方法：Sprague-Dawley（SD）大鼠分为4组：肠I / R组，两个法舒地尔预处理组（7.5 mg / kg和15 mg / kg）和对照组。评估肠和肺的组织病理学;确定了肺实质中的髓过氧化物酶（MPO）和超氧化物歧化酶（SOD）的水平。测量血清肿瘤坏死因子-α（TNF-α）和白介素-6（IL-6）。通过蛋白质印迹法测量eNOS和P-ERM表达。结果：肠I / R诱发肺和肠损伤，其特征是组织学损伤和BALF蛋白显着增加。与对照组相比，I / R组的血清TNF-α，IL-6和肺MPO活性显着增加，而SOD活性则下降。观察到强阳性的P-ERM表达，而eNOS表达弱。法舒地尔给药后，损伤得到缓解。与I / R组相比，血清TNF-α，IL-6，肺MPO和P-ERM表达显着降低，而SOD活性和eNOS表达显着增加。意义：Rho激酶在肠I / R引起的肺损伤的发病机理中起关键作用。盐酸法舒地尔对Rho激酶途径的抑制作用可预防肺损伤。

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