银杏叶提取物对大鼠实验性结肠炎肿瘤坏死因子-α表达的影响

目的观察银杏叶提取物对三硝基苯磺酸灌肠诱导大鼠实验性结肠炎肿瘤坏死因子-α(TNF-α)的影响及其作用机制。方法大鼠随机分为正常对照组、三硝基苯磺酸模型组、阳性药物对照组、EGB组4组。用三硝基苯磺酸灌肠诱导大鼠实验性结肠炎,评估结肠组织大体形态和组织学评分;生化法检测大鼠肠组织谷胱苷肽过氧化物酶(GSH-Px)活性及一氧化氮(NO)含量;免疫组化检测肠组织TNF-α,核因子-κBp65(NF-κBp65)蛋白表达。逆转录聚合酶链反应(RT-PCR)检测肠组织诱生型一氧化氮合酶(iNOS)表达。结果EGB组大体形态和组织学评分较模型组明显下降,GSH-Px活性明显增高,NO含量明显减少,结肠黏膜TNF-α,NF-KBp65和iNOS表达明显降低。结论EGB可能通过抑制TNF-α的表达和NF-κBp65及iNOS的激活从而抑制炎症级联来保护TNBS诱导的实验性结肠炎。

Effect of Ginkgo biloba extract on tumor necrosis factor-alpha expression in TNBS-induced colitis in rats

Aim To investigate the effects of Ginkgo biloba extract(EGB)on tumor necrosis factor-alpha(TNF-α)in TNBS-induced colitis in rats and its mechanisms.Methods Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid(TNBS).Wistar rats were randomly divided into four groups,10 in each:normal group,model group,5-aminosalicylic acid(5-ASA group)and Ginkgo biloba extract group(EGB group).The levels of nitric oxide(NO),and glutathion peroxide(GSH-Px)were measured by biochemical methods.The expressions of TNF-α and nuclear factor kappaBp65(NF-κBp65)in the colon tissues of colitis rats were detected by means of immunohistochemistry.The expressions of induce nitric oxide synthase(iNOS)in the colon tissues of colitis rats were detected by reverse transcription polymerase chain reaction(RT-PCR).The effects of EGB on colonic inflammation and macroscopic and histological damage were evaluated as well.Results Compared with the model group,treatment with EGB for 4 weeks significantly reduced colon macroscopic and histological damage,elevated the activities of GSH-Px and reduced the contents of NO,inhibited the protein expressions of TNF-α andNF-κBp65,and decreased the mRNA levels of iNOS in the colon tissues of experimental colitis.Conclusions The probable mechanisms of EGB was that it ameliorated inflammatory injury in TNBS-induced colitis in rats by its reduction of TNF-α,NF-κBp65 and iNOS levels.Then EGB could curb the inflammatory cascade effects of inflammatory mediators to protect ulcerative colitis.