SB203580防治新生大鼠高氧肺损伤的作用与机制

目的:探讨P38 MAPK特异性抑制剂SB203580对新生大鼠高氧肺损伤产生保护作用的机制。方法:160只新生大鼠随机分为空气对照组、高氧肺损伤组、高氧肺损伤+SB203580组和高氧肺损伤+生理盐水组,建立模型。作用12,24,72 h和1周后,分别处死大鼠。取72 h的左肺以Western blot法检测P38 MAPK的表达情况,取4个时相点的右肺检测肺组织中丙二醛(MDA)含量、总抗氧化能力(TAOC)。结果:72 h时高氧肺损伤组和高氧肺损伤+生理盐水组P38 MAPK呈阳性表达,肺组织MDA含量随时间延长呈上升趋势,在各时相点均高于空气对照组和高氧肺损伤+SB203580组(P<0.01);TAOC随时间延长逐渐降低,在各时相点均低于空气对照组和高氧肺损伤+SB203580组(P<0.01)。结论:SB203580可能通过阻断P38 MAPK表达,进而通过减轻机体的氧化应激反应来减轻新生大鼠高氧肺损伤。

Protection of P38MAPK Inhibitor SB203580 from Hyperoxia-Induced Lung Injury in New-Born Rats

Objective: To investigate the mechanism of protection from hyperoxia-induced lung injury in new-born rats by SB203580,a P38 MAPK specific inhibitor. Methods: A total of 160 new-born rats were divided into air control group,hyperoxia-induced lung injury group,hyperoxia-induced lung injury SB203580 group and hyperoxia-induced lung injury sodium chloride group randomly.After 12 h,24 h,72 h and 1week,rats were executed respectively.Left lungs at 72 h were harvested to detect the expression of P38 MAPK by Western blot,and right lungs at the 4 time points were harvested to detect the concentrations of malondiadehyde(MDA) and total anti-oxygen capability(TAOC).Results: At 72 h,P38 MAPK was expressed positively in hyperoxia-induced lung injury group and hyperoxia-induced lung injury sodium chloride group.The concentrations of MDA in the two groups increased time-dependently,and were higher than those in the air control group and hyperoxia-induced lung injury SB203580 group at the each time point(all P<0.01).In the two groups,the TAOC decreased time-dependently and were lower than those in the air control group and hyperoxia-induced lung injury SB203580 group at the each time point(all P< 0.01).Conclusion: Hyperoxia-induced lung injury in new-born rats can be relieved by the treatment of SB203580 through inhibiting the oxidative stress.