| 克霉唑抗肝缺血-再灌注损伤凋亡机制的研究* |
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| 引用本文： | 许静,陈杰,罗子玲,官碧琼,何炳洪,孙萍萍,袁芳. 克霉唑抗肝缺血-再灌注损伤凋亡机制的研究*[J]. 骨科, 2015, 34(4): 432-435 |
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| 作者姓名： | 许静 陈杰 罗子玲 官碧琼 何炳洪 孙萍萍 袁芳 |
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| 作者单位： | 1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006,1.南方医科大学附属第三医院药剂科,广州510630;2.中山大学附属第一医院药学部,广州510080;3.广东药学院药科学院药理系,广州510006 |
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| 摘 要： | 目的观察孕烷X受体(PXR)诱导药克霉唑对肝脏缺血-再灌注损伤后肝细胞凋亡影响,并探讨其机制。方法建立大鼠肝脏缺血-再灌注模型,32只雄性SD大鼠随机分为假手术组,模型对照组和克霉唑小剂量组、大剂量组进行肝缺血-再灌注损伤。TUNEL法检测肝组织中凋亡细胞,Western blot检测肝脏CYP3A1、Bcl-2、Bax、PARP表达水平。结果克霉唑小剂量组、大剂量组与模型对照组比较,细胞凋亡数减少,组织损伤减轻,凋亡细胞百分率明显降低,Bcl-2/Bax比值明显升高,抑制PARP剪切,提示有较好的抗凋亡作用,均差异有统计学意义;作为PXR特异性强诱导药克霉唑,与假手术组比,能明显诱导CYP3A1基因表达。结论PXR特异性强诱导药克霉唑可能通过促进Bcl-2表达及抑制Bax表达而拮抗肝细胞凋亡,从而减轻肝脏缺血-再灌注损伤,也与抑制PARP剪切有关。
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| 关 键 词： | 克霉唑 肝细胞 损伤,缺血-再灌注 细胞凋亡 孕烷X受体 |
Study of Clotrimazole on Cell Apoptosis in Rat Liver After Ischemia-reperfusion Injury |
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| Abstract: | ObjectiveTo investigate the effect of clotrimazole on apoptosis of hepatic cells after ischemia-reperfusion injury and its mechanism.MethodsHepatic ischemia-reperfusion rat model was established.Thirty-two male Sprague-Dawley rats were randomly allocated into sham-operated group,model control group,low dose clotrimazole group and high dose clotrimazole group.Apoptosis in hepatic tissue was assessed by TUNEL method.Protein expression levels of CYP3A1,Bcl-2,Bax and PARP were measured by Western blotting.ResultsAs compared with model control group,the apoptosis rate,tissue injury,activity of plasma enzymes and the Bax/Bcl-2 expression ratio were reduced in low and high dose clotrimazole groups.The apoptotic index in both clotrimazole-treated groups was lower than that of model control group with statistically significant difference.CYP3A1 expression was significantly induced by clotrimazole compared to the sham-operated group.ConclusionClotrimazole may inhibit apoptosis of hepatic cells by up-regulating Bcl-2 and down-regulating Bax,thus produce a protective effect on hepatic ischemia-reperfusion injury and it is also related to the inhibition of PARP shear. |
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| Keywords: | Clotrimazole Hepatocytes Injury,Ischemia-reperfusion Apoptosis Pregnane X receptor |
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