Qigu capsule alleviates dexamethasone-induced muscle dysfunction through mitochondrial biogenesis

Objective: To explore the potential molecular mechanism of Qigu capsule (，QGC) improve the functional performance of skeletal muscle.

Methods: The primary components of QGC were analyzed using high-performance liquid chromatography (HPLC). Muscle dysfunction was established in male C57BL/6 mice treated with dexamethasone (1 mg/kg body weight, i.p., six weeks). Rotarod test, mitochondrial ultrastructure, respiratory chain complex V activity, Succinate Dehydrogenase (SDH) activity, adenosine triphosphate (ATP) content, and Reactive Oxygen Species (ROS) levels were assessed. The mitochondrial biogenesis-related protein expressions were analyzed using Western blot or polymerase chain reaction (PCR).

Results: QGC treatment enhanced Rotarod test performance. Additionally, QGC significantly alleviated dexamethasone-induced mitochondrial damage, reduced mitochondrial swelling, increased respiratory chain complex enzyme activity, SDH activity, ATP content, and decreased ROS levels. PCR and western blot results revealed that QGC enhanced mitochondrial biogenesis via adenosine 5'-monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ coactivator 1-alpha (PGC-1α) signaling pathway.

Conclusions: QGC ameliorates dexamethasone-induced skeletal muscle dysfunction by activating AMPK/ PGC-1α, which might be developed as a therapeutic agent for treating age-related muscle weakness.

AMP-activated protein kinases; Qigu capsule; muscle weakness; organelle biogenesis; peroxisome proliferator-activated receptor gamma coactivator 1-alpha; sarcopenia.