Pneumocyte apoptosis after total hepatic ischemia-reperfusion in rats and the effect of propofol on apoptosis
Xian Yun-shu
Abstract
Xian Yun-shu
Abstract
Objective To explore pneumocyte apoptosis induced by total hepatic ischemia-reperfusion(I/R) in rats and the effect of propofol on cell apoptosis and its related mechanism.Methods 24 rats were randomly divided into 3 groups(n=8 in each group):propofol group,I/R group and sham-operation group.Total hepatic I/R was produced by occlusion of hepatic helium for 30 minutes,and the occlusion was then released for reperfusion.In propofol group and I/R group,propofol(50 mg/kg)or normal saline of the same volume was administered intraperitoneally 10 min before ischemia,the animals were killed at 1h of reperfusion.In sham-operation group,the hepatic helium wasn't occluded,normal saline was injected and the animals were killed at corresponding time.Then the lung tissue was taken for determation of W/D ratio,MDA content,SOD activity,apoptotic cells,and histological examination.Results (1)Compared with that in sham-operation group,the W/D ratio,apoptotic index and MDA content were all significantly increased(P0.01),and the SOD activity was significantly decreased(P0.01).Histological examination revealed that the alveolar architecture was destroyed with interstitial thickening and neutrophil infiltration in I/R group.(2)Compared with that in I/R group,the W/D ratio,apoptotic index and MDA content were all significantly decreased(P0.01),and the SOD activity was significantly increased(P0.01)in propofol group,and the histological changes was less severe.Conclusion Cell apoptosis may play an important role during the development of lung injury induced by total hepatic I/R.Propofol can inhibite pneumocyte apoptosis induced by total hepatic I/R,which might be mediated by anti-oxidation.
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Objective To explore pneumocyte apoptosis induced by total hepatic ischemia-reperfusion(I/R) in rats and the effect of propofol on cell apoptosis and its related mechanism.Methods 24 rats were randomly divided into 3 groups(n=8 in each group):propofol group,I/R group and sham-operation group.Total hepatic I/R was produced by occlusion of hepatic helium for 30 minutes,and the occlusion was then released for reperfusion.In propofol group and I/R group,propofol(50 mg/kg)or normal saline of the same volume was administered intraperitoneally 10 min before ischemia,the animals were killed at 1h of reperfusion.In sham-operation group,the hepatic helium wasn't occluded,normal saline was injected and the animals were killed at corresponding time.Then the lung tissue was taken for determation of W/D ratio,MDA content,SOD activity,apoptotic cells,and histological examination.Results (1)Compared with that in sham-operation group,the W/D ratio,apoptotic index and MDA content were all significantly increased(P0.01),and the SOD activity was significantly decreased(P0.01).Histological examination revealed that the alveolar architecture was destroyed with interstitial thickening and neutrophil infiltration in I/R group.(2)Compared with that in I/R group,the W/D ratio,apoptotic index and MDA content were all significantly decreased(P0.01),and the SOD activity was significantly increased(P0.01)in propofol group,and the histological changes was less severe.Conclusion Cell apoptosis may play an important role during the development of lung injury induced by total hepatic I/R.Propofol can inhibite pneumocyte apoptosis induced by total hepatic I/R,which might be mediated by anti-oxidation.
Key concepts: Propofol, Apoptosis, Saline, Ischemia, Reperfusion injury, Medicine, Lung, Occlusion