【摘要】 目的 通过建立炎症相关性结直肠癌小鼠模型,探讨岩白菜素在炎症相关性结直肠癌中的抑制作用。方法 使用AOM/DSS建立炎症相关性结直肠癌模型,将小鼠分为空白组、模型组和岩白菜素组,给药过程中记录各组小鼠个体质量、死亡情况,比较各组小鼠结直肠肿瘤数目及负荷,通过HE染色观察各组小鼠结直肠组织病理,通过实时定量PCR检测IL-6、IL-17和IL-23的表达,通过Westem-blotting检测pSTAT3的表达,通过免疫组化检测CD8~+T细胞数量,通过免疫荧光检测肿瘤相关巨噬细胞(TAM)数量。结果 AOM/DSS诱发结直肠癌可造成小鼠体质量下降和死亡率增高,岩白菜素可改善小鼠体重,降低结直肠肿瘤的发生,减少肿瘤组织中炎性因子和pSTAT3表达,同时升高CD8~+T细胞数量,降低肿瘤浸润TAM细胞数量。结论 岩白菜素抑制AOM/DSS诱导的小鼠炎症相关性结直肠癌的发生发展,其机制与抑制TAM相关。更多还原

【Abstract】 Objectives To explore the inhibitory effects of Bergenin on colitis associated colon cancer(CAC) through the establishment of mice model with AOM/DSS.Methods AOM/DSS was given to mice to induce colon cancer.All mice were divided into control group,AOM/DSS group and AOM/DSS+Bergenin group.Body weight and death rate were recorded once a week.Colonorectal tumor number and load were compared among all groups.For pathological assessment,colon tissues were stained with HE.The expression levels of IL-6,IL-17 and IL-23 were determined by qPCR.Western blotting was used to analyse the expression of STAT3 and p-STAT3.CD8~+T cells were determined by immunohistochemical staining.Tumor associated macrophages(TAM) were analysed by immunofluorcsence staining for CD68.Results Dergenin improved the weight loss and death rate in AOM/DSS induced CAC mice model.Bergenin decreased the colonorectal tumor number and tumor load,downregulated the expression level of IL-6,IL-17 and IL-23.Bergenin decreased the phosphorylation of STAT3 in colonic tissues.Notably,Bergenin significantly decreased the infiltration of TAM in cancer rissue.Conclusion Bergenin inhibits the development of inflammatory colorectal cancer induced by AOM/DSS in mice,and its mechanism is related to the inhibition of Tam.更多还原