Pristimerin, a triterpenoid, has exhibited potential anti-inflammatory and anti-tumor activities. Nevertheless, the role and mechanism of pristimerin in intestinal inflammation and colon cancer require further investigation. Here, we found that pristimerin protected mice from dextran sulfate sodium (DSS)-induced colitis, restoring epithelial damage and reducing tissue inflammation and inflammatory cell infiltration. In addition, pristimerin dramatically reduced the number and size of the tumors in a azoxymethane (AOM)/DSS-induced colitis-associated colorectal cancer (CAC) model. Furthermore, we found that pristimerin suppressed Wnt/β-catenin signaling by RNA-Seq. Pristimerin inhibited Wnt/β-catenin signaling via activation of GSK3β, thereby suppressing Wnt target gene expression in colon cancer HCT116 and HT-29 cells. In HCT116 colon cancer xenografts and APCmin/+ mice, which undergo spontaneous intestinal tumorigenesis, administration of pristimerin reduced the tumor progression and decreased the expression of phosphorylated GSK3β Ser 9, β-catenin, cyclin D1 and c-Myc. These results suggest that pristimerin is a potent agent for preventing colon inflammation and carcinogenesis.

中文翻译：

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Pristimerin通过抑制炎症反应和Wnt /β-catenin信号传导抑制大肠癌。

Pristimerin是一种三萜类化合物，已显示出潜在的抗炎和抗肿瘤活性。然而，普利司林蛋白在肠道炎症和结肠癌中的作用和机制尚需进一步研究。在这里，我们发现普里司特林保护小鼠免受硫酸葡聚糖钠（DSS）诱导的结肠炎的侵害，恢复了上皮的损害并减少了组织炎症和炎性细胞浸润。此外，普利司特林显着减少了由乙氧基甲烷（AOM）/ DSS诱导的结肠炎相关大肠癌（CAC）模型中肿瘤的数量和大小。此外，我们发现普里司汀通过RNA-Seq抑制Wnt /β-catenin信号转导。Pristimerin通过激活GSK3β抑制Wnt /β-catenin信号传导，从而抑制结肠癌HCT116和HT-29细胞中Wnt靶基因的表达。在HCT116结肠癌异种移植和APCmin / +小鼠中，它们会自发地进行肠道肿瘤形成，普里司汀的给药减少了肿瘤的进展，并降低了磷酸化的GSK3βSer 9，β-catenin，cyclin D1和c-Myc的表达。这些结果表明，普里司特林是预防结肠炎症和致癌作用的有效剂。