[目的]探讨马齿苋多糖(POP)干预三硝基苯璜酸(TNBs)诱导大鼠实验性结肠炎(UC)的作用机制。[方法]48只雄性SD大鼠随机分为正常组、模型组、POP组,每组16只。用5%2,4,6 TNBs 100 mg/kg灌肠建立大鼠UC模型,第3天开始,除正常组外,各组分别给予0.85%氯化钠、POP处理,连续给药7 d后处死。应用透射电镜、免疫组化染色分别分析结肠淋巴细胞凋亡及凋亡相关基因Bcl-2、Bax、Caspase-3蛋白表达;应用黏蛋白染色分析结肠黏膜修复情况,综合评价POP的作用机制。[结果]模型组结肠黏膜淋巴细胞凋亡不明显,凋亡相关基因Bcl-2蛋白表达呈上升趋势,Bax、Caspase-3蛋白表达呈明显下降趋势,且黏蛋白合成分泌减少,杯状细胞数目减少;予POP干预后,结肠黏膜淋巴细胞凋亡明显,凋亡相关基因Bax/Bcl-2之间比例>1,作为凋亡终末的关键酶即Caspase-3表达亦呈上升趋势,且黏蛋白合成分泌增加,2组比较差异有统计学意义(P<0.01)。[结论]POP可能通过上调Bax、Caspase-3的表达,下调Bcl-2的表达,诱导结肠黏膜淋巴细胞凋亡;刺激结肠黏蛋白分泌,促进结肠黏膜修复,发挥缓解大鼠UC的效应。 [Objective] To explore the mechanism of purslane polysaccharide (POP) in interventional trinitrophenylhydrazine (TNBs)-induced experimental colitis (UC) in rats. [Methods] Forty-eight male SD rats were randomly divided into normal group, model group, and POP group, with 16 rats in each group. Rat UC models were established with 5% 2,4,6 TNBs 100 mg/kg enema. Starting from the third day, each group was given 0.85% sodium chloride and POP, except for the normal group, and sacrificed after 7 days of continuous administration. . Transmission electron microscopy and immunohistochemical staining were used to analyze the apoptosis of lymphocytes and the expression of apoptosis-related genes Bcl-2, Bax, and Caspase-3 in colonic neoplasms. Mucosal staining was used to analyze the repair of colonic mucosa and the mechanism of POP was comprehensively evaluated. [Results] The apoptosis of colonic mucosal cells in the model group was not obvious, and the expression of apoptosis-related gene Bcl-2 protein showed an upward trend. The expression of Bax and Caspase-3 protein showed a downward trend, and the synthesis and secretion of mucin decreased. The number of goblet cells was decreased. After the intervention of POP, the apoptosis of colonic mucosal lymphocytes was obvious, and the ratio of apoptosis-related genes Bax/Bcl-2 was >1. The expression of Caspase-3, which is the key enzyme in the terminal apoptosis, also showed an upward trend, and the viscosity was increased. Protein synthesis and secretion increased, the difference between the two groups was statistically significant (P<0.01). [Conclusion] POP ​​may up-regulate the expression of Bax and Caspase-3, down-regulate the expression of Bcl-2, induce apoptosis of colonic mucosal lymphocytes, stimulate the secretion of mucin in the colon, promote the repair of colonic mucosa, and exert the effect of relieving UC in rats.