CYP8B1 (Cytochrome P450 Family 8 Subfamily B Member 1)

In vitro Cell Counting Kit 8 assays and in vivo orthotopic liver tumor model analyses showed that CYP8B1 restores sorafenib sensitivity in resistant HC, suggesting its potential as a therapeutic target...Our findings indicate that the CYP8B1/PAK4 axis is important in HCC progression and elucidate the mechanism by which BAs promote HCC. Thus, CYP8B1 is a potential therapeutic target for the clinical treatment of HCC.

Furthermore, the pro‑apoptotic protein Bax was upregulated, while the anti‑apoptotic protein Bcl‑2 was downregulated. In conclusion, CYP8B1 holds promise as a potential prognostic target for HCC.

Furthermore, DCFH-DA staining was adopted to visualize reactive oxygen species (ROS). In conclusion, for the first time, we found that FXR overexpression alleviates LCA-induced cholestasis by regulating bile acid metabolism and inhibiting NLRC4 inflammasome activation, providing a novel therapeutic strategy for drug development targeting the FXR-NLRC4 axis.

In this review, the necessity of incorporating age as a crucial element in understanding the disparities in outcomes for EO‑GC cases in public datasets was discussed. Furthermore, this insight may be useful for targeted early personalized clinical interventions to improve patient prognosis and survival rates in EO‑GC cases.

In conclusion, LRG1 emerges as a potential biomarker for prognosis and immunotherapy responsiveness in both pan-cancer and KIRC contexts. This study provides a theoretical foundation for further research on the therapeutic potential of target regulating LRG1 in cancer treatment.

Here, we developed a new model of MASH with HCC using mice with human-like BA composition and found that HFHSD and elevated hepatic CDCA synergistically increased the risk of MASH with HCC.

Taken together, HRCC improved MCD-induced NAFLD through anti-inflammatory mechanisms and by increasing antioxidative activities. Additionally, HRCC might alter gut microbiome to change hepatic bile acid contents, exerting beneficial effects for the treatment of NAFLD.

This study revealed the protective effect of APS on NAFLD was associated with the regulation on BA profiles, and proved the potential anti-NAFLD effect of THDCA, highlighting the involvement of BA metabolism in efficacy of herb-derived polysaccharides on metabolism.

These changes collectively contributed to improved BA efflux from the liver and enhanced renal elimination of BAs. In conclusion, ACA demonstrated its potential to ameliorate ANIT-induced liver damage by inhibiting BA synthesis and promoting both BA efflux and renal elimination pathways, thus, restoring BA homeostasis.

Hepatic deletion of Cp effectively remodels bile acid metabolism by upregulating Cyp7a1 and Cyp8b1, which subsequently leads to enhanced bile acid synthesis and notable alterations in bile acid profiles. In conclusion, our studies elucidate the crucial involvement of Cp in NASH, highlighting its significance as a promising therapeutic target for the treatment of this disease.

Overall, our study suggests that an HFHC diet after cholecystectomy promotes intestinal inflammation by exacerbating the gut microbiome and BA metabolism dysbiosis in cholecystectomy. Our study also provides useful insights into the maintenance of intestinal health after cholecystectomy through dietary or probiotic intervention strategies.