Yan Ma,Zhengnan Jiang,Hai Xie,Jian Wang,Minni Li,Huifang Ge,Wenbin Li,Zhongwen Xie,Daxiang Li,Xueling Gao,Hongyan Wang
Fermented oxidation fresh tea (FOFT) is a unique dark tea produced by a single strain of Eurotium cristatum , and its impact on obesity has not been extensively studied. Here, we investigated the anti-obesity and metabolic benefits of FOFT using a HFD-induced obesity mouse model. The HFD-fed mice or ND-fed mice were orally administered with FOFT for 12 weeks. The results showed that FOFT invention significantly suppressed body weight gain, ameliorated liver and adipocyte morphology, and improved glucolipid metabolism and intestinal homeostasis imbalance in HFD-fed mice. Notably, FOFT administration caused no adverse effects in ND mice, indicating its safety at tested doses. Moreover, FOFT restored intestinal microbiome dysbiosis and elevated the short-chain fatty acid levels. This gut microbiome shift was associated with reduced systemic inflammation and attenuated hepatic lipid accumulation. These findings suggest that FOFT, as a novel functional food, holds great promise for resistance to obesity and its comorbidities.
Breast cancer is a significant threat to life and health, which needs more safe and effective drugs to be explored. Teadenol B is a characteristic chemical component of microbial fermented tea. This study discovered that teadenol B could exhibit obvious inhibitory effects on all four different clinical subtype characteristics of breast cancer cells. Proteomic studies show that deoxycytidine triphosphate deaminase (DCTD), which could block DNA synthesis and repair DNA damage, had the most significant and consistent reduction in all four types of breast cancer cells with the treatment of teadenol B. Considering MDA-MB-231 cells exhibit poor clinical prognosis and displayed substantial statistical differences in KEGG pathway enrichment analysis results, we investigated its impact on the size and growth of MDA-MB-231 triple-negative breast tumors transplanted into nude mice and demonstrated that teadenol B significantly suppressed tumor growth without affecting body weight significantly. Finally, we found that the conversion of LC3-I to LC3-II in MDA-MB-231 increased significantly with teadenol B treatment. This proved that teadenol B could be a strong autophagy promotor, which explained the down-regulation of DCTD to some extent and may be the potential mechanism underlying teadenol B’s anti-breast cancer effects. This finding provides new evidence for drinking fermented tea to prevent breast cancer and highlights the potential of teadenol B as a novel therapeutic option for breast cancer prevention and treatment, necessitating further investigations to clarify its exact target and the details involved.Keywords:teadenol B;breast cancer;autophagy
危险品化学品经营许可证（带存储）