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目的探讨地塞米松和法舒地尔(fasudil)对油酸致小鼠急性肺损伤的影响及ROCK(Rho-associated coiledcoil forming kinase)在其中的作用。方法采用油酸致C57小鼠急性肺损伤模型,观察伤后24h各组肺组织病理及肺含水率、ROCK活性、ROCK1和ROCK2蛋白含量及IL-1βmRNA的变化。结果地塞米松和法舒地尔均可显著减轻油酸肺组织中炎性细胞浸润、肺出血等病理变化,降低肺含水率(P<0.05),抑制肺组织ROCK活性(P<0.05),降低IL-1βmRNA的表达水平;地塞米松对ROCK1的表达水平无影响,但可增强ROCK2的表达,法舒地尔对ROCK1和ROCK2的表达水平均无影响。结论地塞米松和法舒地尔均可通过抑制肺组织内炎性细胞浸润明显减轻油酸引起的急性肺损伤,而地塞米松的治疗作用可能与对其ROCK活性的抑制有关。
Objective To investigate the effect of dexamethasone and fasudil on acute lung injury induced by oleic acid in mice and the role of ROCK-associated coiledcoil forming kinase. Methods The acute lung injury model induced by oleic acid in C57 mice was used to observe the changes of lung histopathology and lung water content, ROCK activity, ROCK1 and ROCK2 protein contents and IL-1βmRNA in all groups. Results Both dexamethasone and fasudil could significantly reduce the pathological changes of inflammatory cell infiltration and pulmonary hemorrhage, reduce the lung water content (P <0.05) and inhibit the activity of ROCK in lung tissue (P <0.05) Dexamethasone had no effect on the expression of ROCK1, but increased the expression of ROCK2. Fasudil had no effect on the expression of ROCK1 and ROCK2. Conclusion Both dexamethasone and fasudil can significantly reduce oleic acid-induced acute lung injury by inhibiting the infiltration of inflammatory cells in lung tissue, whereas the dexamethasone treatment may be related to the inhibition of ROCK activity.