Ginsenosides: potential therapeutic source for fibrosis-associated human diseases

Area of Science:

• Pharmacology
• Pathology
• Natural Products

Background:

• Tissue fibrosis, a hallmark of chronic diseases, involves fibroblast activation and excessive extracellular matrix deposition, leading to organ dysfunction.
• Significant unmet clinical needs persist for effective antifibrotic therapies.
• Recent research highlights the antifibrotic potential of ginsenosides across various animal models.

Purpose of the Study:

• To review the therapeutic prospects of ginsenosides in fibrosis-related human diseases.
• To consolidate findings from animal models for potential clinical translation.
• To identify key molecular targets modulated by ginsenosides in fibrosis.

Main Methods:

• Literature review of studies investigating ginsenosides and fibrosis.
• Analysis of molecular mechanisms targeted by ginsenosides.
• Evaluation of efficacy in preclinical animal models of fibrosis.

Main Results:

• Ginsenosides demonstrate efficacy in attenuating fibrosis in various animal models.
• Potential therapeutic targets include Caveolin-1, ILs, TSP-1, LXRs, Nrf2, miR-27b, PPARδ-STAT3, LKB1-AMPK, and TGF-β1/Smads.
• Ginsenosides suppress inflammation, collagen deposition, epithelial-mesenchymal transition (EMT), and myofibroblast activation.

Conclusions:

• Ginsenosides represent a promising therapeutic strategy for combating tissue fibrosis.
• Targeting specific pathways with ginsenosides can mitigate fibrotic processes.
• Further exploration of ginsenosides may yield novel antifibrotic drugs for human diseases.