Effect of resveratrol on activity of NADPH oxidase during acute lung injury induced by intestinal ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of resveratrol on the activity of NADPH oxidase during acute lung injury induced by intestinal ischemia-reperfusion (I/R) in rats.Methods Thirty-two pathogenfree healthy female Sprague-Dawley rats,weighing 180-230 g,were divided into 4 groups (n =8 each) using a random number tablesham operation group (Sham group),intestinal I/R group (I/R group),vehicle group (Veh group) and resveratrol group (Res group).Intestinal I/R was produced by occlusion of the superior mesenteric artery for 75 min followed by 4 h of reperfusion.In group Res,resveratrol 15 mg/kg was intraperitoneally injected for 5 consecutive days before establishment of the model and at 15 min before ischemia.The equal volume of vehicle (0.5％ alcohol) was intraperitoneally injected in group Veh.The equal volume of normal saline was intraperitoneally injected in Sham and I/R groups.At the end of reperfusion,the rats were sacrificed and the lung was removed for microscopic examination of pathologic changes which were scored and for determination of wet/dry weight ratio (W/D ratio),malondialdehyde (MDA) content and superoxide dismutase (SOD) activity (by colorimetric method) and expression of NADPH oxidase subunits (gp91phox and p47phox) in lung tissues (by Western blot).Results Compared with group Sham,pathologic scores,W/D ratio and MDA content were significantly increased,the expression of gp91phox and p47phox was up-regulated,and the activity of SOD was decreased in I/R and Veh groups (P＜0.05).Compared with I/R and Veh groups,pathologic scores,W/D ratio and MDA content were significantly decreased,the expression of gp91phox and p47phox was down-regulated,and the activity of SOD was increased in group Res (P＜0.05).Conclusion The mechanism by which resveratrol reduces intestinal I/R-induced acute lung injury is related to inhibiting NADPH oxidase-mediated oxidative stress response of rats.