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[目的]探讨溃结通方(KJT)对葡聚糖硫酸钠(DSS)诱导的SD大鼠溃疡性结肠炎(UC)的干预作用。[方法]以40只SD大鼠为研究对象,采用DSS自由饮水建立UC模型,造模成功后,再随机分为模型组、KJT高剂量组、KJT低剂量组、SASP组,行中药(高剂量15g/kg、低剂量5g/kg)、SASP(0.3g/kg)灌胃治疗2周,观察SD大鼠疾病活动度指数(DAI),结肠黏膜情况及血清白细胞介素(IL-1β)、肿瘤坏死因子(TNF-α)水平。[结果](1)KJT明显降低DSS诱导的UC大鼠DAI评分(P<0.001);(2)KJT可改善模型大鼠的肠道病理损伤,减少炎性细胞浸润,黏膜上皮排列整齐,肠腺规则,杯状细胞丰富;(3)KJT抑制模型大鼠血清IL-1β、TNF-α(P<0.05)促炎因子的释放,且IL-1β水平与KJT呈剂量相关性。[结论]KJT高、低剂量组和SASP组均可改善DSS诱导的SD大鼠UC炎症病变,其中KJT高剂量组呈现更好的治疗效应趋势,优于低剂量组及SASP组。
[Objective] To explore the intervention of Kuijie tong (KJT) on dextran sulfate sodium (DSS) -induced ulcerative colitis (UC) in SD rats. [Methods] Forty SD rats were used as experimental subjects. UC models were established by drinking water DSS. After successful modeling, they were randomly divided into model group, KJT high dose group, KJT low dose group, SASP group, Dose of 15g / kg, low dose of 5g / kg) and SASP (0.3g / kg) for 2 weeks. The disease activity index (DAI), colonic mucosa and serum IL- , Tumor necrosis factor (TNF-α) levels. [Results] (1) KJT significantly decreased the DAI score of UC rats induced by DSS (P <0.001). (2) KJT could improve the pathological injury of intestinal tract, reduce the infiltration of inflammatory cells, arrange the mucosal epithelium neatly, (3) The release of proinflammatory cytokines (IL-1β, TNF-α (P <0.05)) in KJT-inhibited rats and the dose-dependent relationship between IL-1β and KJT. [Conclusion] KJT high and low dose groups and SASP group can improve DSS induced UC inflammatory lesions in SD rats, and the KJT high dose group showed a better therapeutic effect trend, which was better than the low dose and SASP groups.