Methylprednisolone Experimental Ischemia And Reperfusion Injury Of Rat Lung

Objective To investigate the effect of methylprednisolone(MP) onpneumocyte apoptosis and IκB-αduring pulmonary ischemia reperfusioninjury(LIRI) in rats and to study the possible role of methylprednisoloneon pneumocyte apoptosis.Methods Forty-two male Sprague-Dawley rats used for unilateral lungischemia/reperfusion model were randomly divided into threegroups(fourteen rats in each group): sham operation group(Sh group),ischemia/reperfusion group(IR group) and methylprednisolone group(MPgroup). Each group has two subgroups of three hours and six hours. IRinjury consisted of 45 minutes of lung cross-clamping following 3hours(or 6 hours) of reperfusion. MP with 30mg/kg was injected byintraperitoneal injection in MP group. Apoptosis rate in lung tissue wasdetected by the way of Annexin-V-PI in flow cytometer. Expression ofIκB-αin lung tissue was observed by immunohistochemical stain andimage analysis. The index of quantitative assessment of histologic lunginjury(IQA), the wet to dry weight ratio(W/D),the pathological andultrastructure changes of lung tissue were also measured.Results Apoptosis rate, W/D, IQA of lung tissue were significantly higherin IR group than in Sh group(P＜0.01) while the expression of IκB-αinlung tissue was obviously lower in IR group than in Sh group(P＜0.01).Apoptosis rate of lung tissue was significantly correlated with IQA level of lung tissue(r=0.9714, P=0.0003), but it had negative correlationbetween apoptosis rate and IκB-αlevel of lung tissue(rS=-0.8929,P=0.0068). MP group had more significant changes in apoptosis rate, theexpression of IκB-α, W/D, IQA of lung tissue than IR group(P＜0.05). Thepathological and ultrastructure changes of lung tissue were better in MPgroup than in IR group.Conclusions Celluar apoptosis and IκB-αplay a more important role inthe pathological and physiological process of LIRI. In early periodapoptosis rate changes following the change of inflammatory reaction.MP inhibits the apoptosis of LIRI, extenuates the degree of LIRI by thepossible mechanism of decreasing the activation of IκB-αin early periodof LIRI.