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目的探讨p38丝裂原活化蛋白激酶(p38MAPK)抑制剂在葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎大鼠肠道动力障碍中的作用。方法 34只Sprague-Dawley大鼠用随机数字表法随机分成4组:正常对照组(正常组,n=8),DSS模型组(DSS组,n=8),DSS+生理盐水(NS)组(DSS+NS组,n=9),DSS+SB203580干预组(SB203580组,n=9)。除正常组外,所有大鼠每日饮用5%DSS溶液,SB203580组大鼠在饮用5%DSS溶液72 h以后,每天予以SB203580(1 mg/kg体质量)进行腹腔注射,观察各组大鼠的疾病活动指数(DAI),以酚红法测定大鼠结肠传输功能。结果 1 DSS组和DSS+NS组大鼠的DAI评分明显高于正常组,SB203580组DAI评分明显降低,但仍然高于正常组(P<0.05),DSS组和DSS+NS组之间差异无统计学意义(P>0.05)。2与正常对照组比较,DSS组和DSS+NS组大鼠的结肠传输功能明显延迟,经SB203580干预后,其结肠传输功能明显改善(P<0.05),DSS组和DSS+NS组之间差异无统计学意义(P>0.05)。结论 SB203580能阻断p38MAPK信号转导通路,改善DSS诱导的结肠炎症,从而改善结肠传输功能。
Objective To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) inhibitor in intestinal motility disorders induced by dextran sodium sulfate (DSS) in rats with ulcerative colitis. Methods Thirty-four Sprague-Dawley rats were randomly divided into 4 groups: normal control group (n = 8), DSS model group (n = 8), DSS + NS group DSS + NS group, n = 9), DSS + SB203580 intervention group (SB203580 group, n = 9). Rats in SB203580 group were given intraperitoneal injection of SB203580 (1 mg / kg body weight) daily for 72 hours after drinking 5% DSS solution, except for the normal group. Rats in each group were dosed with DSS solution Of disease activity index (DAI), measured by the phenol red colonic transit function in rats. Results The DAI scores of DSS group and DSS + NS group were significantly higher than those of normal group. The DAI score of SB203580 group was significantly lower than that of normal group (P <0.05). There was no difference between DSS group and DSS + NS group Statistical significance (P> 0.05). Compared with the normal control group, the colonic transit function of rats in DSS group and DSS + NS group was significantly delayed. The colonic transit function was significantly improved after SB203580 intervention (P <0.05), and there was no significant difference between DSS group and DSS + NS group No statistical significance (P> 0.05). Conclusion SB203580 can block the p38MAPK signal transduction pathway and improve colonic inflammation induced by DSS, so as to improve colonic transit function.