芒果苷对实验性结肠炎小鼠的保护作用

Mangiferin protects mice from experimental colitis

目的探讨芒果苷对小鼠实验性溃疡性结肠炎(ulcerative colitis,UC)的保护作用和机制。方法将C57BL/6小鼠随机分为4组(n=10):正常对照组、模型组、柳氮磺胺吡啶组(SASP,350 mg·kg-1,腹腔注射)以及芒果苷组(MA,50 mg·kg-1,灌胃)。除正常对照组外,其他组小鼠均以饮用水中添加葡聚糖硫酸钠(dextran sodium sulfate,DSS)造模。SASP组和MA组分别于造模前2 d每日给予SASP和MA直到实验结束。于造模7 d处死小鼠,对结肠行HE染色后进行组织损伤和炎性细胞浸润评分,以ELISA方法检测结肠黏膜髓过氧化物酶(MPO)活性和TNF-α水平。结果模型组小鼠的病理损伤和评分、MPO活性和TNF-α水平均明显高于正常对照组,MA组上述指标比模型组明显改善,但改善效果不如SASP组明显。结论芒果苷可以减轻实验性UC小鼠的结肠黏膜损伤,其UC保护作用机制可能与其抑制中性粒细胞浸润和减少炎症细胞因子产生有关。

Aim To investigate the protective effect of Mangiferin （MA） on experimental ulcerative colitis （UC） and its possible mechanism. Methods Mice were randomly divided into 4 groups： vehicle treatment group, DSS treatment group, DSS ＋ SASP treatment group and DSS ＋ MA treatment group. Mice UC model was induced by adding 4% dextran sulfate sodium （DSS） into drinking water for 7 consecutive days. Sul- fasalazine （SASP） and MA were administered, respec- tively, 2 d prior to and throughout the DSS treatment. After mice sacrifice, the entire colon was excised and stained with hematoxylin-eosin （ HE ） for histological evaluation. Histological score of HE-stained sections was assessed. The activity of myeloperoxidase （MPO） and the level of TNF-α in colon mucosa were measured by ELISA method. Results Mice treated with vehicle alone exhibited intact mypt-villus structures. DSS ad- ministration resulted in a damage of endothelial struc- tures and a severe inflammation infiltration. By con- trast, SASP or MA administration to DSS-exposed mice resulted in significant attenuation of the mueosal dam- age and histologic inflammation. In addition, a signifi- cant increase in the aetivity of MPO and the level ofTNF-α in colon were observed in mice exposed to DSS as compared to vehicle treatment mice. Administration either with SASP or MA resulted in a marked reduction in MPO activity and TNF-α level in mucosa. Conclu- sion The current study demonstrates a protective effect of MA on DSS-induced UC through an inhibition of leukocyte infiltration and inflammatory cytokines pro- duction.