文章摘要
许朝龙,邬善敏,苗志钊,等.白藜芦醇对胆道梗阻再通大鼠肝功能的保护作用[J].安徽医药,2016,20(1):30-33.
白藜芦醇对胆道梗阻再通大鼠肝功能的保护作用
Protective effect of resveratrol on liver injury in rats after recanalization of biliary obstruction
投稿时间:2015-09-09  
DOI:
中文关键词: 白藜芦醇  梗阻性黄疸  再通  沉默信息调控因子  过氧化物酶体增殖物剂激活受体α  核因子-κB
英文关键词: resveratrol  obstructive jaundice  recanalization  SIRT1  PPARα  NF-κB
基金项目:
作者单位E-mail
许朝龙 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060  
邬善敏 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060 15327278328@163.com 
苗志钊 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060  
赵凯亮 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060  
陈飞 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060  
范迪欢 武汉大学人民医院肝胆腔镜外科,湖北 武汉 430060  
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中文摘要:
      目的 研究白藜芦醇(Res)对胆道梗阻再通大鼠肝损害的保护作用及机制。方法 雄性Wistar大鼠60只,随机分为4组,即A组:假手术组,B组:梗阻性黄疸模型组,C组:梗阻性黄疸模型+胆道再通组,D组:梗阻性黄疸+胆道再通 +Res干预组。连续给药7 d,实验结束后检测各组大鼠血清中总胆红素(TBIL)、直接胆红素(DBIL)、丙氨酸氨基转氨酶(ALT)水平;RT-PCR检测肝组织沉默信息调控因子1(SIRT1)mRNA的表达,Western blot检测肝组织SIRT1蛋白和核因子-κB(NF-κB)蛋白表达,免疫组化检测过氧化物酶体增殖物激活受体α(PPARα)蛋白在肝脏中的表达,原位末端标记(TUNEL)法检测肝细胞凋亡。结果 与假手术组比较,模型组血清ALT水平升高,SIRT1 mRNA及蛋白、PPARα蛋白表达降低,NF-κB蛋白表达升高,细胞凋亡率升高(P<0.05);而造模后胆道再通组与模型组比较,血清ALT水平降低,SIRT1 mRNA及蛋白、PPARα蛋白表达增加,NF-κBp蛋白表达降低,细胞凋亡率降低(P<0.05);白藜芦醇组与C组比较:血清ALT水平降低,SIRT1 mRNA及蛋白、PPARα蛋白表达增加,NF-κBp蛋白表达降低,细胞凋亡率降低(P<0.05)。结论 Res可能通过激活SIRT1抑制NF-κB,发挥抗炎、抗凋亡作用,通过促进PPARα的表达发挥抗氧化作用,从而减轻胆道梗阻再通大鼠的肝损害,促进肝功能恢复。
英文摘要:
      Objective To explore the protective effect of resveratrol (Res) on liver injury in rats after recanalization of biliary obstruction. Methods Sixty healthy male Wistar rats were randomized into four groups:sham group (group A), obstructive jaundice one week group (group B), obstructive jaundice one week and recanalization one week+NS group (group C), obstructive jaundice one week and recanalization one week+Res group (group D). The levels of total bilirubin(TBIL),direct bilirubin(DBIL) and serum alanine aminotransferase(ALT) were measured. Real-time polymerase chain reaction (RT-PCR) was performed to determine the mRNA expression of silent information regulator 1(SIRT1). The expression of the SIRT1 and nuclear factor-κB (NF-κB) proteins were detected by Western blot. Immunocytochemical assay was performed to examine peroxisome proliferator activated receptor-alpha (PPARα) protein. Hepatocellular apoptosis was examined by terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) method. Results Compared with group A, in group Bthe level of ALT was higher, the expressions of SIRT1 mRNA and protein and the PPARα protein were lower, and the NF-κB protein and the rate of hepatocellular apoptosis were higher(P<0.05). Compared with group B, in group Cthe level of ALT was lower, the expression of SIRT1 mRNA and protein and the PPARα protein were higher, and the NF-κB protein and the rate of hepatocellular apoptosis were lower(P<0.05). Compared with group C, in group Dthe level of ALT was lower, the expressions of SIRT1 mRNA and protein and the PPARα protein were higher, and the NF-κB protein and the rate of hepatocellular apoptosis were lower(P<0.05).Conclusion The Res could resist inflammation and apoptosis by activating the SIRT1 which probably inhibits the expression of NF-κB protein, and palys an antioxidant role by promoting the expression of PPARα in rats after recanalization of biliary obstruction, so that it could alleviate liver damage.
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