CAJ | 학술논문

目的探讨丙泊酚对内毒素诱导的肺损伤及细胞凋亡的影响.方法将18只SD雄性大鼠随即分为对照组、盐水组、丙泊酚组各6只,一次性雾化吸入内毒素(1 mg/kg)诱导急性肺损伤后,丙泊酚组大鼠立即给予负荷剂量丙泊酚5 mg/kg,继以丙泊酚10mg (kg·h)维持6 h,对照组及盐水组予以等量生理盐水代替.分别以HE染色观察病理变化、湿干重比(W/D)检测肺水肿程度、TUNEL染色检测细胞凋亡、western blot检测Bax及Bcl-2表达变化、荧光法检测caspase-3活性.结果与对照组相比,盐水组病理可见问质水肿,大量中性粒细胞浸润等炎症改变,W/D增加(P＜ 0.01),凋亡细胞数及caspase-3活性明显增高(P＜0.01),Bax表达增高及Bcl-2表达降低;与盐水组相比,丙泊酚组HE染色仅少量中性粒细胞浸润,W/D降低(P＜0.05),凋亡细胞数及caspase-3活性明显降低(P＜0.01),Bax表达下降及Bcl-2表达增加.结论丙泊酚可以通过抑制细胞凋亡的发生从而保护LPS诱导的ALI.
목적 탐토병박분대내독소유도적폐손상급세포조망적영향.방법 장18지SD웅성대서수즉분위대조조、염수조、병박분조각6지,일차성무화흡입내독소(1 mg/kg)유도급성폐손상후,병박분조대서립즉급여부하제량병박분5 mg/kg,계이병박분10mg (kg·h)유지6 h,대조조급염수조여이등량생리염수대체.분별이HE염색관찰병리변화、습간중비(W/D)검측폐수종정도、TUNEL염색검측세포조망、western blot검측Bax급Bcl-2표체변화、형광법검측caspase-3활성.결과 여대조조상비,염수조병리가견문질수종,대량중성립세포침윤등염증개변,W/D증가(P＜ 0.01),조망세포수급caspase-3활성명현증고(P＜0.01),Bax표체증고급Bcl-2표체강저;여염수조상비,병박분조HE염색부소량중성립세포침윤,W/D강저(P＜0.05),조망세포수급caspase-3활성명현강저(P＜0.01),Bax표체하강급Bcl-2표체증가.결론 병박분가이통과억제세포조망적발생종이보호LPS유도적ALI.
Object To investigate the effect of propofol on lipopolysaccharide (LPS)-induced acute lung injury and apoptosis in rats.Methods 18 SD male rats were randomly and equally divided into a control group,an LPS + normal saline (NS) group,and an LPS + propofol group.After anesthetization,the rats were intratracheally given a single dose of aerosolized LPS (1 mg/kg) and the control rats were intratracheally given normal saline.Then,the rats in the LPS + propofol group were iutravenously administrated propofol 5 mg/kg followed by continuous infusion 10 mg/(kg · h) for 6 hours.The rats in the control group and the LPS + NS group received a same volume of NS.All rats were sacrificed to detect interstitial edema and histopathology changes respectively by wet-to-dry weight ratio (W/D) and hematoxylin-eosin (HE) staining.To further investigate the protective effects of propofol on apoptosis,TUNEL staining,fluorometric assay,and western blot were respectively used for measuring the number of apoptotic cell,caspase-3 activity,and apoptosis relative proteins including Bax and Bcl-2.Results Comparing with the control group,the LPS + NS group got interstitial edema.exhibited siguificant lung injury characterizing by deterioration of histopathological characteristics,had a higher W/D,apoptosis in ALI significantly reflected by massive TUNEL staining-positive cells,higher caspase-3 activity (P ＜ 0.01),and up-regulation of Bax and down-regulation of Bcl-2 (P ＜ 0.01).After propofol treatment,these alterations were partially inhibited.Conclusions These results indicated that propofol treatment ameliorates LPS-induced ALI inhibiting apoptosis.