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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
Astragalus polysaccharides decrease muscle wasting through Akt/mTOR, ubiquitin proteasome and autophagy signalling in
Lu Lu1, Yan-Feng Huang2, De-Xiu Chen1
1Department of Traditional Chinese Medicine, ZhuJiang Hospital, Southern Medical University, Guangzhou 510280, China; School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China; Department of Nephrology, Southern Medical University TCM-Integrated Hospital, Guangzhou 510515, China.
Astragalus polysaccharides (APS) combat muscle wasting in nephrectomized rats by improving protein metabolism and reducing inflammation. APS influences key molecular pathways, including Akt/mTOR, and may target amino acid transporters like SLC38A2.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Radix Astragali polysaccharides (APS) show potential for improving muscle mass.
- Mechanisms underlying APS effects on muscle require further investigation.
Purpose of the Study:
- To investigate the molecular mechanisms of APS in mitigating muscle wasting.
- To evaluate APS effects in a rat model of chronic kidney disease (5/6 nephrectomy).
Main Methods:
- 5/6 nephrectomy or sham operation in Sprague-Dawley rats, treated with or without 2% APS for 155 days.
- Analysis of body weight, muscle fiber characteristics, protein metabolism, inflammatory markers (TNF-α, IL-15, CRP), and oxidative stress markers (MDA, SOD).
- In vivo and in vitro assessment of Akt/mTOR, ubiquitin-proteasome system, autophagy signaling (Atg7, LC3B-II/LC3B-I), and amino acid transporters (SLC38A2).
Main Results:
- APS treatment alleviated weight loss and improved protein metabolism in nephrectomized rats.
- APS normalized serum levels of pro-inflammatory and oxidative stress markers.
- Molecularly, APS restored Akt/mTOR signaling, ubiquitin-proteasome components (MAFbx, MuRF1), autophagy markers (Atg7, LC3B-II/LC3B-I), and SLC38A2 expression.
Conclusions:
- APS ameliorates muscle wasting in nephrectomized rats via modulation of Akt/mTOR, ubiquitin-proteasome, and autophagy pathways.
- SLC38A2 is identified as a potential molecular target for APS-mediated muscle protection.
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