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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.

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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.

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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.