当归汤多糖对溃疡性结肠炎的改善作用及机制初步研究

Preliminary study on the improvement effect and mechanism of Danggui Decoction polysaccharide eextracts on ulcerative colitis

关键词:  当归汤多糖  溃疡性结肠炎  免疫调节  氧化应激

Key words:  Danggui Decoction polysaccharide extracts  ulcerative colitis  immune regulation  oxidative stress

摘要:

[目的] 探讨当归汤多糖改善溃疡性结肠炎（UC）的作用和机制。[方法] 构建2，4，6-三硝基苯磺酸（TNBS）诱导的UC大鼠模型，通过疾病活动指数（DAI）、结直肠宏观损伤评分、苏木精-伊红（HE）染色的结直肠病理评分，评价当归汤多糖对UC的干预作用，并检测结直肠组织氧化应激指标[超氧化物歧化酶（SOD）、丙二醛（MDA）、髓过氧化物酶（MPO）]、脾细胞刺激指数及白细胞介素（IL）-2和干扰素-γ（IFN-γ）水平。采用RAW264.7细胞模型，检测当归汤多糖对NO生成的影响。取正常及UC大鼠脾细胞，研究当归汤多糖对刀豆蛋白A（Con-A）刺激下脾细胞增殖的影响，对其作用机制进行初步研究。[结果] 动物实验中，模型组大鼠出现黏液便、血便，上述指标均较对照组存在显著性差异。与模型组相比，美沙拉嗪组和当归汤多糖高剂量组DAI值、宏观损伤评分、组织病理学评分、脾细胞刺激指数、IL-2和IFN-γ水平、MDA含量、MPO活力均显著降低、SOD活力均显著增强。细胞实验中，与空白组相比，当归汤多糖能剂量依赖地增加RAW264.7细胞的一氧化氮（NO）水平，且显著低于1 μg/mL脂多糖（LPS）刺激RAW264.7细胞的NO水平；与模型组相比，当归汤多糖对Con-A刺激下正常大鼠脾细胞增殖具有明显促进，对Con-A刺激下TNBS诱导的UC大鼠的脾细胞增殖有抑制作用。[结论] 当归汤多糖对TNBS诱导的UC大鼠的病症有一定的改善作用，其作用机制可能与调节免疫，抑制氧化应激有关。

Abstract:

[Objective] To explore the effect and mechanism of Danggui Decoction polysaccharide extracts(DGDPE) in improving ulcerative colitis (UC).[Methods] AUC rat model induced by 2,4,6-Trinitrobenzenesulfonic acid(TNBS) was established to evaluate the effects of DGDPE on UCthrough disease activity index (DAI),colorectal macroscopic injury score,and HE staining colorectal pathology score. RAW264.7 cell model was used to detect the influence of DGDPE on NO production. Spleen cells of normal and UC rats were taken to study the effect of DGDPE on the proliferation of spleen cells under the stimulation with Con-A,and study on mechanism by detecting colorectal tissue oxidative indicators (SOD,MDA,MPO),IL-2 and IFN-γlevels,andspleen cell proliferation.[Results] Rats in the model group had mucus and bloody stools,and the above indicators were significantly different from those in the control group. Compared with the model group,the DAI index,macroscopic injury score,colorectal pathology score,spleen cell stimulation index,IL-2 and IFN-γ levels,MDA content,and MPO activity significantly decreased,and SOD activity significantly increased. Compared with the blank group,DGDPE could significantly increase the production of NO in RAW264.7 cells. But the NO levels of all DGDPE treated groups were significantly lower than that of the positive control stimulated by 1 μg/mL LPS. Compared with the model group,DGDPE could significantly promote the proliferation of normal rat spleen cells and inhibit the proliferation of UC rat spleen cells under the stimulation with Con-A.[Conclusion] DGDPE has an improvement effect on TNBS-induced UC in rats,and its mechanism may be related to the regulation of immunity inhibition and alleviation of oxidative stress.