March 3, 2026Open Access

Bruceine D ameliorates cholestatic liver injury by selectively modulating bile acid synthesis and activating FXR–SHP signaling

Key Points

Bruceine D alleviates cholestatic liver injury through specific modulation of bile acid synthesis.
The treatment results in a less hepatotoxic bile acid profile and reduced inflammation and fibrosis.
Analysis shows restoration of FXR-dependent signaling as a key mechanism behind Bruceine D's effects.
This therapy could be a promising option for cholestatic liver diseases, but further validation is needed.

Abstract

BD ameliorates cholestatic liver injury by selectively inhibiting classical BA synthesis, quantitatively remodeling the BA pool toward a less hepatotoxic profile, and suppressing inflammation and fibrosis through functional restoration of FXR-dependent feedback signaling. Its synthesis-centered mechanism and favorable short-term safety profile support BD as a promising therapeutic candidate for cholestatic liver diseases.

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