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作 者:钟江鹏[1] 李登欣[2] 李石[1] 李杰[1] 徐静[1]
机构地区:[1]潍坊医学院,山东省潍坊市261042 [2]潍坊市人民医院消化内科,山东省潍坊市261042
出 处:《世界华人消化杂志》2009年第36期3679-3683,共5页World Chinese Journal of Digestology
基 金:山东省科技发展计划基金资助项目;No.2005GG4402004~~
摘 要:目的:探讨己酮可可碱(PTX)对三硝基苯磺酸(TNBS)诱导的大鼠溃疡性结肠炎(UC)肠黏膜炎性细胞因子TNF-α及IL-1β表达的影响.方法:应用三硝基苯磺酸(TNBS)/乙醇灌肠制备大鼠UC的模型.实验设正常对照组(C组)、TNBS损伤组(T组)、PTX治疗组(D组),从造模后第3天开始给予D组大鼠PTX腹腔注射治疗,C组、T组则注入等量生理盐水,bid,连用5d.观察疾病活动指数(DAI).处死大鼠,应用RT-PCR(逆转录-聚合酶链反应)方法半定量检测技术,对UC大鼠结肠黏膜中TNF-α、IL-1β mRNA表达进行测定.结果:TNBS损伤组大鼠肠黏膜TNF-α、IL-1β mRNA的表达及DAI评分明显高于正常对照组和PTX治疗组(6.85±2.78 vs 0.45±0.11,1.85±2.01;1.02±0.16 vs 0.61±0.08,0.74±0.16;0.95±0.17 vs 0.57±0.07,0.64±0.13,均P<0.05),而PTX治疗组与对照组相比则无明显差异(均P>0.05).结论:UC的发生过程中炎性细胞因子TNF-α及IL-1β表达升高;己酮可可碱可能通过降低炎性细胞因子TNF-α及IL-1β的表达而发挥其干预作用.AIM: To investigate the effects of pentoxifylline (PTX) on the expression of tumor necrosis factor-alpha(TNF-α) and interleukin-1β(IL-1β) in trinitrobenzene sulfonic acid (TNBS)-induced ulcerative colitis (UC) in rats. METHODS: UC was induced in rats with TNBS and ethanol. The rats were randomly divided into three groups: normal group (C), TNBS group (T), and PTX group (D). Three days after UC was induced, the rats in the PTX group received a PTX injection every 12 hours for five consecutive days, while the remaining two groups received an injection of distilled water. The disease activity index (DAI) was evaluated daily. The expression of TNF-α and IL-1β mRNAs was measured by reverse transcription-polymerase chain reaction (RT-PCR) RESULTS: Compared with the normal group and the PTX group, the expression of TNF-α and IL-1β mRNAs and DAI in the TNBS group were markedly higher (6.85±2.78 vs 0.45±0.11 and 1.85±2.01; 1.02±0.16 vs 0.61±0.08 and 0.74±0.16; and 0.95±0.17 vs 0.57±0.07 and 0.64±0.13, respectively; all P 〈 0.05). No significant differences were noted in the expression levels of TNF-α and IL-1β mRNAs and DAI between the normal group and the PTX group (all P 〉 0.05). CONCLUSION: The expression of proinflammatory factors TNF-α and IL-1β mRNAs increases in rat ulcerative colitis. PTX exerts protective effects against UC possibly by downregulating the expression of TNF-α and IL-1β mRNAs.
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