PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
May 18, 2026Journal of Functional Foods0 citationsOpen Access

Auricularia auricula polysaccharides attenuate ventricular remodeling in mice by suppressing oxidative stress and apoptosis via activation of the Keap1/Nrf2/HO-1 pathway

View Full Paper
XGXiaofeng GaoSLShuang LiYBYali Bao

Key Points

  • This research aims to explore the effects of Auricularia auricula polysaccharides on ventricular remodeling and the underlying mechanisms involved.
  • In vivo interventions with AAP (100 and 150 mg/kg) on isoproterenol-induced mouse models.
  • Assessment of cardiac function, myocardial hypertrophy, and oxidative stress markers.
  • Proteomic profiling and validation of the Keap1/Nrf2/HO-1 pathway activation.
  • AAP significantly improved cardiac function and reduced myocardial hypertrophy and fibrosis in ISO-challenged mice.
  • Activation of the Keap1/Nrf2/HO-1 pathway was confirmed with promotion of Nrf2 nuclear translocation (p<0.01).
  • AAP effectively inhibited oxidative stress markers (MDA/ROS) and decreased apoptosis indicators (cleaved caspase-3, p<0.05).

Abstract

Ventricular remodeling (VR) represents a critical pathological process in heart failure, for which therapeutic strategies remain limited. Auricularia auricula , an edible and medical fungus, contains bioactive polysaccharides (AAP), but its role in VR is unclear. This study investigated the cardioprotective effects and underlying mechanism of AAP on isoproterenol (ISO)-induced VR. Structural analysis revealed AAP as a porous aggregated polysaccharide. In vivo , AAP (100 and 150 mg/kg) significantly improved cardiac function and attenuated myocardial hypertrophy, fibrosis, and ultrastructural damage in ISO-challenged mice. Mechanistically, AAP suppressed oxidative stress (reducing MDA/ROS, enhancing GSH/SOD) and cardiomyocyte apoptosis (decreasing TUNEL + cells and cleaved caspase-3). Proteomic profiling and molecular validation demonstrated that AAP consistently activated the Keap1/Nrf2/HO-1 pathway, promoting Nrf2 nuclear translocation while downregulating Keap1 both in vivo and in ISO-stimulated H9C2 cells. These findings identify AAP as a potential functional food ingredient for preventing pathological cardiac remodeling through modulation of antioxidant defense. • AAP alleviates ISO-induced cardiac dysfunction and structural remodeling in mice. • Proteomics and molecular assays confirm AAP activates the Keap1/Nrf2 antioxidant pathway. • AAP inhibits cardiomyocyte apoptosis, oxidative stress and fibroblast activation. • AAP shows potential as functional food ingredient for preventing pathological cardiac remodeling.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Gao et al. (2026) studied this question.

synapsesocial.com/papers/6a0aac6d5ba8ef6d83b6fdcehttps://doi.org/10.1016/j.jff.2026.107342
Ask AI
Helpful
Bookmark
Share
View Full Paper