20(S)-ginsenoside Rg3 promotes myoblast differentiation and inhibits myotube atrophy by protecting mitochondrial function via AMPK/FoxO3 pathway in high glucose-induced model

Abstract

Background High glucose is usually considered to be the factor that induces tissue damage and cell dysfunction during diabetes. Muscle, as an important target organ for insulin, is particularly be attacked by high glucose. 20(S)-ginsenoside Rg3 (S-Rg3) has shown protective effect on vascular smooth muscle in diabetes. But whether S-Rg3 has protective effect on skeletal muscle injury caused by high glucose has not been reported. Methods Myoblast differentiation were measured by Western blot and immunofluorescence staining. Myotube atrophy were measured by Giemsa staining and Western blot. Flow cytometry, Seahorse and Western blot were used to detect mitochondrial function. Drosophila exposed to high sucrose diet (HSD) to establish an in vivo model of muscle damage. Trehalose and triglyceride levels were detected by spectrophotometry. Mef2 mRNA level was detected by RT-PCR. Muscle atrophy were detected by toluidine blue staining. Climbing distances were determined by climbing assay. The morphological structure of mitochondria was observed by transmission electron microscope. AMP-activated protein kinase (AMPK) and Forkhead box O3 (FoxO3) were analyzed by Western blot. UAS-AMPK RNAi Drosophila were used to verify the AMPK/FoxO3 pathway in vivo. Results S-Rg3 promoted myoblast differentiation and inhibited muscle atrophy injured by high glucose. S-Rg3 recovered mitochondrial function