Background:Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies
for sarcopenia is highly desired. Ampelopsin (AMP), as one of the major bioactive components in Rattan tea, exerts a large number of physiological and pharmacological actions such as
anti-inflammatory, antioxidant, hepatoprotective and neuroprotective functions. However, its function for the regulation of sarcopenia is rarely reported. The aim of this study is to explore the
preventive efficacy of AMP on D-galactose (D-gal)-induced sarcopenia and corresponding mechanisms.
Methods:Forty Sprague-Dawley rats were randomly divided into four groups including control, D-gal induction, and D-gal induction coupled with AMP treatment and AMP treatment alone
groups. The model of sarcopenia was established by subcutaneous injection of D-gal at the dose of 200 mg/kg for 42 days in male SD rats. The model rats were treated with AMP at doses of 100 and 200
mg/kg for 28 days after D-gal injection with saline administration as the normal control. After AMP treatment, the ratio between skeletal muscle and body weight, histopathological characteristics and
senescence-associated β-galactosidase (SA-β-gal) staining were evaluated. Mitochondrial morphology and autophagic vacuoles in gastrocnemius were observed by transmission electron microscopy. The
expression of proteins was detected by Western blotting.
Results:The ratio between gastrocnemius and body weight revealed a significant decrease after 42 days D-gal induction when compared with that from the control. More importantly, AMP
treatment could abolish the decrease in muscle-to-body weight ratio and mitigate the damage of the cells in gastrocnemius in a dose-dependent manner. AMP pre-treatment significantly reversed
D-gal-induced apoptosis, thereby revealing as enhanced Bax and Caspase-3, and reduced Bcl-2. In addition, the pre-treatment of AMP could result in the declined expression of atrophy markers such as
atrogin-1 and MuRF1 in gastrocnemius. Furthermore, the pretreatment with AMP revealed the obvious activation of autophagy due to the increased LC3-II/LC3-I ratio.
Conclusions:AMP can delay the formation of sarcopenia by activating autophagy and reduce the apoptosis in gastrocnemius.