摘要
背景：白芍总苷（TGP）具有抗炎、免疫调节等作用，其对炎症性肠病是否具有治疗作用尚不清楚。目的：探讨TGP对大鼠实验性结肠炎的影响及其可能机制。方法：50只大鼠以三硝基苯磺酸（TNBS）／乙醇溶液灌肠诱导结肠炎模型，分为结肠炎模型组、低、中、高剂量TGP组（25、50、100mg／kgTGP）和阳性药物对照组（100mg／kg奥沙拉秦）。10只大鼠作为正常对照组（0．9％NaCl溶液灌肠）。实验期间评估各组疾病活动指数（DAI）；干预2周后行结肠大体损伤指数（CMDI）和组织学损伤指数（TDI）评分，以酶联免疫吸附测定（ELISA）检测血清肿瘤坏死因子-α（TNF-α）和白细胞介素-10（IL-1O）水平，以免疫组化方法检测结肠组织磷酸化p38丝裂原活化蛋白激酶（p—p38MAPK）表达。结果：与结肠炎模型组相比，高剂量TGP组实验期间DAI均值显著降低（P＜0．01）；中、高剂量TGP组CMDI和TDI显著降低，血清TNF-α水平降低，IL-10水平升高，结肠组织p-p38MAPK表达降低（P＜0．05）。高剂量TGP的疗效与奥沙拉秦无明显差异。结论：TGP可能通过抑制p38MAPK激活，抑制TNF-α分泌，促进IL—10分泌，改善免疫调节紊乱，从而减轻TNBS诱导的大鼠实验性结肠炎的症状和结肠炎性损伤。
Background：The total glucosides of paeony （TGP） have the function of anti-inflammation and immunoregulation, but its therapeutic effect on inflammatory bowel disease is still uncertain. Aims： To investigate the effect of TGP on experimental colitis in rats and its potential mechanism. Methods： Colitis model was induced in 50 rats by rectal administration of trinitrobenzene sulfonie acid （TNBS） dissolved in ethanol. Ten model rats each were treated with 25, 50 and 100 mg/kg TGP, respectively, 10 model rats served as model control group, and 10 model rats were treated with 100 mg/kg olsalazine as drug controls. Other 10 rats receiving 0.9% NaCl solution served as normal controls. Disease activity index （DAI） was evaluated during the intervention. After 2-week intervention, the colonic macroscopic damage index （CMDI） and tissue damage index （TDI） were evaluated, the serum levels of tumor necrosis factor-or （TNF-α） and interleukin-10 （IL-10） were determined by enzyme-linked immunosorbent assay （ELISA）, and the colonic expression of phosphorylated p38 mitogen-activated protein kinase （p-p38MAPK） was determined by immunohistochemical method.Results： Compared with model control group, DAI in high-dose TGP group during the intervention decreased significantly （P〈0.01）; CMDI and TDI, as well as the serum level of TNF-α and the colonic expression of p-p38MAPK in moderate- and high-dose TGP groups decreased significantly, while the serum level of IL-10 increased significantly （P〈0.05）. No statistically significant differences were found between high-dose TGP group and olsalazine group. Conclusions： TGP can attenuate the symptoms and colonic inflammatory damage of TNBS-induced experimental colitis in rats. The mechanism may be related to the inhibition of p38MAPK activation, down-regulation of TNF-α, up-regulation of IL-10 and improvement of immunoregulation.
出处
《胃肠病学》
2009年第3期154-158,共5页
Chinese Journal of Gastroenterology
