Quercetin prevents sarcopenia by reversing oxidative stress and mitochondrial damage

Abstract

This study investigates the effectiveness of quercetin (QUE) in preventing sarcopenia via the PI3K/AKT signaling pathway. Thirty SD rats were categorized into three groups: a young control group (Y), an old control group (O), and an old QUE-supplemented group (O + QUE). Body weight and grip strength were monitored weekly during the experiment. Soleus and gastrocnemius muscle weights, gastrocnemius tissue pathological examination, cell apoptosis, and mitochondrial damage were evaluated using HE, TUNEL staining, electron microscopy, and JC-1 staining. Biochemical assays and molecular biology techniques (qPCR and Western blot) were used to assess oxidative stress markers and the expression of sarcopenia-related genes and proteins. QUE supplementation increased muscle weight and improved grip strength in aged rats. Furthermore, QUE supplementation alleviated tissue damage, apoptosis, enhanced antioxidant capacity, and decreased damage to oxidative stress and mitochondria in the gastrocnemius of old rats. Molecular assessments revealed downregulation of muscle degradation markers (MuRF1, Atrogen-1, Bnip3) and upregulation of PI3K/AKT pathway proteins, suggesting a mechanistic pathway through which QUE mitigates sarcopenia. QUE maybe modulate the PI3K/AKT pathway to alleviate oxidative stress, mitochondrial damage, and muscle degradation due to aging, highlighting its potential as a therapeutic agent against sarcopenia.