目的:探讨马齿苋水提物对溃疡性结肠炎(Ulcerative colitis,UC)的保护作用。方法:利用葡聚糖硫酸钠(Dextran sulfate sodium,DSS)诱导C57BL/6复制UC模型,将小鼠随机分为6组,分别为正常组,DSS模型组,SASP对照组,马齿苋低、中、高剂量组(100,200 mg/kg和400 mg/kg),每天ig给药1次,记录小鼠体重并统计疾病活动指数(Disease activity index,DAI)评分,连续7天。于第8天,测定结肠长度,测定MDA、SOD以及NO含量,观察结肠病理学形态变化,并测定IL-6,IL-1β与TNF-αm RNA的表达。结果:模型组与正常组比较,小鼠体重,结肠长度及SOD有显著降低(P〈0.05),而DAI评分,MDA、NO含量以及TNF-α,IL-6与IL-1βm RNA的表达有明显升高(P〈0.05)。而马齿苋水提物中、高组与模型组比较,小鼠的体重,结肠长度以及SOD含量均有显著性提高(P〈0.05),结肠组织病理损伤有所改善,DAI评分MDA、NO含量以及TNF-α,IL-6与IL-1βm RNA的表达均有明显降低(P〈0.05)。结论:马齿苋水提物对UC具有保护作用,可能与改变SOD、NO与MDA而抑制氧化应激反应及下调TNF-α,IL-6与IL-1β等细胞因子m RNA的表达而降低炎症反应有关。
Objective: To purslane the protective effects of aqueous extract from Portulacaoleracea L.(AEP) on ulcerative colitis(UC). Methods: Use the dextran sulfate sodium(DSS) to establish the UC model, the mice of this study were divided into control group,DSS group, SAPA group(450 mg/kg), and low, medium and high-dose of AEP groups(100 mg/kg, 200 mg/kg and 400 mg/kg). The animals were given relevant medicine intragastrically once and then weighed and disease activity index(DAI) score were recorded daily for 7 days. The colon was excised in day 8, measured the length, detect the level of SOD, NO, MDA by ELISA kit, revealed the morphological features of the colon, and analyze the expression of IL-6, IL-1β and TNF-α. Results: Compared with control group, the body weight, the level of SOD and the colon length were decreased significantly(P〈0.05), the DAI score, the level of NO, MDA, the expression of IL-1β, IL-6 and TNF-α m RNA were significantly increased in model group(P〈0.05). The aqueous extract from Portulacaoleracea L. groups compared with model group couldimprove the pathologic changes, increase the body weight, the level of SOD and the colon length, and decrease the DAI score and the level of NO, MDA, and meanwhile the expression of IL-1β, IL-6 and TNF-α m RNA were also decreased significantly(P〈0.05). Conclusions: The AEP show that the protective effects on DSS induced UC model, and the mechanism may be were inhibit the oxidative stress through MDA, NO, SOD and reduce the inflammatory through the anti the over-expressions of TNF-α, IL-6 and IL-1β.