Effects of Astragalus polysaccharide on skeletal muscle mitochondria in mice with chronic fatigue

HUANG Yan-feng; ZHU Da-jian; LU Lu

doi:10.3969/j.issn.1001-9448.2017.12.001

Abstract：Objective To study the effect of Astragalus polysaccharide (APS) on skeletal muscle mitochondria in mice with chronic fatigue.Methods Chronic fatigue model was established by endurance exercise procedure.Forty BALB/c mice were randomly divided into the sedentary group (SED), endurance exercise group (EXE), APS group (SED+APS), and endurance exercise with APS supplementation group (EXE+APS).The exercise capacity was evaluated by index of the forced swimming capacity and forelimb grip strength.The levels of MDA, LDH, SOD and GPx in both serum and skeletal muscle were detected.Expression levels of PGC-1α, MnSOD, p53, Atg7, LC3, and p62 were detected by Western blot.Expression levels of mitochondrial fusion/fission-related mRNAs were detected by qRT-PCR.Results The index of the forced swimming capacity and forelimb grip strength were significantly increased in EXE+APS group (P<0.05, P<0.01).There were moderate negative correlations between endurance capacity and serum LDH, serum MDA levels and muscle tissue MDA levels;and positive correlations between endurance capacity and serum GPx level.Meanwhile, compared with EXE group, the expression levels of oxidative stress-related protein MnSOD and p53 were significantly reduced in the EXE+APS group (P<0.05, P<0.05), while the mitochondrial biogenesis-related protein PGC-1α was significantly increased (P<0.01);and the autophagy-related protein Atg7 and LC3-Ⅱ/LC3-Ⅰ were significantly reduced (P<0.05, P<0.05), as the p62 was significantly increased (P<0.05).Compared with EXE group, the expression of Mnf-1 and Mnf-2 mRNAs was significantly higher in EXE+APS group (P<0.05, P<0.05), while Drp-1 mRNA was significantly lower (P<0.05).Conclusion APS could restore the exercise capacity in mice with chronic fatigue.The molecular mechanism underlying may involve reduction in oxidative stress, mitophagy restoration, mitochondrial biogenesis, and mitochondrial fusion/fission in skeletal muscles.