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Aim:To investigate the protective effect of triptolide (TRI) on ischemia/reperfusion-induced injury of transplanted rabbit lungs and to investigate the mechanismsunderlying the actions of TRI.Methods:We established the rabbit lung trans-plantation model and studied lung injury induced by ischemia/reperfusion andthe inhibitory effect of TRI on NF-kB.The severity of lung injury was determinedby a gradual decline in PvO_2,the degree of lung edema,the increase in themyeloperoxidase (MPO) activity,and the ultrastructural changes of transplantedlungs.The activation of NF-kB was measured by immunohistochemistry.Theincrease in intercellular adhesion molecule-1 (ICAM-1),which is the target gene ofNF-kB,was evaluated by ELISA.Results:After reperfusion,there was a gradualdecline in the PvO_2 level in the control group (group Ⅰ).The level of PvO_2 in thegroup treated with lipopolysaccharide (group Ⅱ was significantly decreased,whereas that of the group treated with TRI (group Ⅲ) was markedly improved(P<0.01).In group Ⅲ,the activity of MPO was downregulated,and the pulmonaryedema did not become severe and the ultrastructure of the donor lung remainednormal.The activity of NF-kB and the expression of ICAM-1 was significantlyincreased in the donor lungs.TRI blocked NF-kB activation and ICAM-1expression.Conclusion:The effects of TRI on reducing injury to donor lungsinduced by ischemia/reperfusion may possibly be mediated by inhibiting theactivity of NF-kB and the expression of the NF-kB target gene ICAM-1.Thus,TRI could be used in lung transplantations for improving the function of donorlungs.
Aim: To investigate the protective effect of triptolide (TRI) on ischemia/reperfusion-induced injury of transplanted rabbit lungs and to investigate the mechanisms underlyingly the actions of TRI.Methods: We established the rabbit lung trans-plantation model and studied lung injury induced by Ischemia/reperfusion andthe inhibitory effect of TRI on NF-kB.The severity of lung injury was determined by a total decline in PvO_2,the degree of lung edema,the increase in themyeloperoxidase (MPO) activity,and the ultrastructural changes of transplanted lungs.The activation Of NF-kB was measured by immunohistochemistry. Theincrease in intercellular adhesion molecule-1 (ICAM-1), which is the target gene ofNF-kB,was evaluated by ELISA.Results:After reperfusion,there was a gradualdecline in the PvO_2 level in The control group (group I).The level of PvO_2 in thegroup treated with lipopolysaccharide (group II was significantly decreased, whereas that of the group treated with TRI (group III) was markedly Improved(P<0.01).In group III,the activity of MPO was downregulated,and the pulmonaryedema did not become severe and the ultrastructure of the donor lung incubationnormal.The activity of NF-kB and the expression of ICAM-1 was significantincreased in The donor lungs.TRI blocked NF-kB activation and ICAM-1expression.Conclusion:The effects of TRI on reducing injury to donor lungsinduced by ischemia/reperfusion may possibly be mediated by inhibiting theactivity of NF-kB and the expression of the NF-kB Target gene ICAM-1.Thus,TRI could be used in lung transplantations for improving the function of donorlungs.