简介:饮食引起的肥胖已被证明会降低Turicibacter的丰度,已知在5-羟色胺信号系统中起作用的属,这与结直肠肿瘤发生有关,使Turicibacter的存在对肠道肿瘤发生的保护具有潜在的影响。最近,牛樟芝(AC),一种原产于台湾的药用真菌,已成为补充和替代癌症治疗的有希望的候选人。据报道,来自AC的小分子和多糖具有促进健康的作用,包括抗癌特性。方法:本研究采用细菌培养,然后进行细胞培养,以确定Turicibacter在结直肠肿瘤发生中的作用,并探讨Turicibacter发酵AC的抗癌机制。结果:Turicibacter发酵和AC多糖的添加导致营养物质和代谢产物的产生显著增加,包括α-酮戊二酸和乳酸(p<0.05)。处理Turicibacter发酵AC多糖更有效地抑制5-羟色胺信号相关基因,包括Tph1,Htr1d,Htr2a,Htr2b,和Htr2c(p<0.05),和Wnt信号相关蛋白和下游基因表达,如磷酸-GSK-3β,活性β-连环蛋白,c-Myc,Ccnd1和Axin2(p<0.05)。此外,它引发了最高的活性氧(ROS)产生,激活PI3K/Akt和MAPK/Erk信号并导致caspase-3表达。相比之下,没有Turicibacter发酵的AC多糖处理效果较小。讨论:我们的研究结果表明,AC多糖有效地抑制肿瘤的血清素和Wnt信号通路,并促进ROS介导的Caco-2细胞凋亡。这些过程通过Turicibacter发酵进一步增强。
Introduction: Diet-induced obesity has been shown to decrease the abundance of
Turicibacter, a genus known to play a role in the serotonin signaling system, which is associated with colorectal tumorigenesis, making the presence of Turicibacter potentially influential in the protection of intestinal tumorigenesis. Recently, Antrodia camphorata (AC), a medicinal fungus native to Taiwan, has emerged as a promising candidate for complementary and alternative cancer therapy. Small molecules and polysaccharides derived from AC have been reported to possess health-promoting effects, including anti-cancer properties. Methods: Bacterial culture followed with cell culture were used in this study to determine the role of Turicibacter in colorectal tumorigenesis and to explore the anti-cancer mechanism of AC with
Turicibacter fermentation. Results:
Turicibacter fermentation and the addition of AC polysaccharide led to a significant increase in the production of nutrients and metabolites, including α-ketoglutaric acid and lactic acid (p < 0.05). Treatment of Turicibacter fermented AC polysaccharide was more effective in inhibiting serotonin signaling-related genes, including Tph1, Htr1d, Htr2a, Htr2b, and Htr2c (p < 0.05), and Wnt-signaling related protein and downstream gene expressions, such as phospho-GSK-3β, active β-catenin, c-Myc, Ccnd1, and Axin2 (p < 0.05). Additionally, it triggered the highest generation of reactive oxygen species (ROS), which activated PI3K/Akt and MAPK/Erk signaling and resulted in cleaved caspase-3 expression. In comparison, the treatment of AC polysaccharide without
Turicibacter fermentation displayed a lesser effect. Discussion: Our findings suggest that AC polysaccharide effectively suppresses the tumorigenic serotonin and Wnt-signaling pathways, and promotes ROS-mediated apoptosis in Caco-2 cells. These processes are further enhanced by
Turicibacter fermentation.