Ginsenoside Re mitigates Aβ_1-42-induced neurotoxicity by promoting autophagy and suppressing NLRP3 inflammasome.

ABSTRACT:

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) accumulation and neuroinflammation. Activation of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome in microglia significantly contributes to AD-associated neuroinflammation and neuronal damage. Ginsenoside Re (G-Re), a major bioactive constituent of Panax ginseng, exhibits anti-inflammatory properties, but its role in modulating inflammasome activation in AD remains unclear.

Methods

This study evaluated the therapeutic potential of G-Re in mice intracerebroventricularly injected with Aβ_1-42 and delineated its molecular mechanisms in complementary cell-based models. We employed behavioral testing, immunohistochemistry, Western blott

SUBMITTER: Madhi I 

PROVIDER: S-EPMC12805552 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature