摘要
背景:传统药物对炎症性肠病疗效不甚理想,寻找新型而有效的药物一直是该领域的研究热点。目的:观察雷公藤红素对三硝基苯磺酸(TNBS)诱导的大鼠结肠炎的保护作用,并初步探讨其可能机制。方法:以TNBS诱导大鼠结肠炎模型,将动物随机分为正常对照组、模型组、助溶剂对照组以及雷公藤红素低剂量组(每天0.5mg/kg)和高剂量组(每天1mg/kg)。以大体和组织学评分评价结肠炎症程度。以免疫组化方法检测结肠组织核因子(NF)-κBp65的表达,以半定量逆转录聚合酶链反应(RT-PCR)检测白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-αmRNA的表达。结果:高、低剂量雷公藤红素均能显著改善结肠组织大体和组织学评分,降低NF-κBp65以及IL-1β、TNF-αmRNA的表达。结论:雷公藤红素对TNBS诱导的大鼠结肠炎具有显著保护作用,抑制促炎细胞因子的产生可能是其主要作用机制之一。
Background: The therapeutic effects of conventional drugs on inflammatory bowel disease (IBD) are not very satisfactory. To seek novel and effective drug is always the hotspot in the study of IBD. Aims: To investigate the protective effects of tripterine on trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats and to explore its possible mechanisms. Methods: Rat colitis model was induced by TNBS enema. Then the rats were randomly divided into 5 groups: normal control group, model group, adjuvant solution control group, low- (0.5 mg/kg per day) and high-dose (1 mg/kg per day) tripterine-treated groups. The severity of colitis was evaluated by macroscopic and microscopic score. The expression of nuclear factor (NF)-kB p65 in the colonic tissues was detected by immunohistochemistry, and the expressions of interleukin (IL)-1β and tumor necrosis factor (TNF)-α mRNA were assessed by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Results: Remarkable efficacy of both low- and high-dose of tripterine was observed in TNBS-induced colitis with decrement of macroscopic and microscopic score and suppression of NF-kB p65, IL-1β mRNA and TNF-α mRNA expressions in the colonic tissues. Conclusions: Tripterine has noticeable protective effects on TNBS-induced colitis in rats, suppression of proinflammatory cytokines may be one of its main mechanisms.
出处
《胃肠病学》
2007年第3期144-147,共4页
Chinese Journal of Gastroenterology