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[Effects of electroacupuncture on proangiogenesis process and protein turnover in a mouse model of sarcopenia]
Zheng-Wei Zhu1, Cheng-Lin Tang1, Xiao-Hong Li2
1College of Traditional Chinese Medicine of Chongqing Medical University, Chongqing 400016, China.
Objective:
To observe the effect of electroacupuncture(EA) on proangiogenesis process and protein turn-over in a mouse model of sarcopenia, so as to explore its potential molecular mechanism anti-aging.
Methods:
Fourteen 30-week-old male SAMP8 mice were randomly divided into a model group (n=7) and an EA group (n=7). Seven anti-rapidly aging SAMR1 mice of the same age were used as the control group (n=7). EA (1 mA, 4 Hz) was applied to bilateral "Zusanli"(ST36) and "Yanglingquan"(GB34) for 20 minutes each time once a day, 6 times a week for 4 weeks. The exhausted running platform was used to test the sports function. Gastrocnemius muscle mass and relative ratio of gastrocnemius muscle mass to body mass were measured. HE staining and transmission electron microscope were used to observe the morphology, and the cross-sectional area of gastrocnemius muscle was calculated. Relative protein expressions of protein kinase B (AKT) , phosphorylated (p) -AKT, mammalian target of rapamycin (mTOR) , p-mTOR, p70 ribosomal protein S6 kinase (p70S6K) , p-p70S6K,hypoxia inducible factor-1α (HIF-1α) and relative mRNA expressions of HIF-1α, vascular endothelial growth factor A (VEGF-A) , muscle RING finger-1 (MuRF-1) and muscle atrophy F-box (MAFbx) were detected by Western blot and real-time fluorescence quantitative PCR, seperatively.
Results:
Compared with the control group, the running time and distance, body mass and gastrocnemius mass, and the ratio of gastrocnemius mass to body mass decreased(P<0.01, P<0.05), cross-sectional area of gastrocnemius, related protein expression of p-AKT,p-mTOR, p-p70S6K and HIF-1α, mRNA expression of HIF-1α and VEGF-A decreased (P<0.01), while mRNA expression of MuRF1 and MAFbx increased (P<0.01) in the model group. Following EA intervention, the running time and distance, body mass and gastrocnemius mass and the ratio of gastrocnemius mass to body mass increased (P<0.05), cross-sectional area of gastrocnemius, related protein expression of p-AKT,p-mTOR, p-p70S6K and HIF-1α, mRNA expression of HIF-1α and VEGF-A were significantly up-regulated (P<0.01), mRNA expression of MuRF1 and MAFbx down-regulated (P<0.01, P<0.05) in the EA group compared with the model group.
Conclusion:
EA may delay the aging muscle atrophy in mice by regulating the gastrocnemius muscle's proangiogenesis process and protein turnover.
Insights
Electroacupuncture (EA) treatment improved muscle mass and function in aged mice with sarcopenia. EA enhanced proangiogenesis and regulated protein turnover, suggesting a potential anti-aging mechanism for muscle health.
Area of Science:
- Gerontology and Regenerative Medicine
- Integrative and Complementary Medicine
- Muscle Physiology and Molecular Biology
Background:
- Sarcopenia, characterized by age-related muscle loss, significantly impacts mobility and quality of life.
- Understanding the molecular mechanisms underlying sarcopenia is crucial for developing effective interventions.
- Electroacupuncture (EA) is a potential therapeutic modality for age-related conditions.
Purpose of the Study:
- To investigate the effects of EA on proangiogenesis and protein turnover in a mouse model of sarcopenia.
- To explore the molecular mechanisms by which EA may exert anti-aging effects on skeletal muscle.
Main Methods:
- Sarcopenic mice (SAMP8) and control mice (SAMR1) were used.
- EA was applied to specific acupoints (ST36, GB34) for 4 weeks.
- Muscle function, mass, morphology, and molecular markers (AKT, mTOR, HIF-1α, VEGF-A, MuRF-1, MAFbx) were assessed.
Main Results:
- Sarcopenic mice exhibited decreased muscle mass, function, and proangiogenesis markers, with increased muscle atrophy markers.
- EA intervention significantly improved muscle mass, function, and proangiogenesis (VEGF-A, HIF-1α).
- EA treatment downregulated muscle atrophy markers (MuRF-1, MAFbx) and modulated key signaling pathways (AKT/mTOR).
Conclusions:
- EA treatment effectively ameliorates age-related muscle atrophy in mice.
- EA influences muscle proangiogenesis and protein turnover, potentially via the AKT/mTOR and HIF-1α pathways.
- EA demonstrates potential as a therapeutic strategy for combating sarcopenia and promoting muscle anti-aging.
