Open Access

Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway

  • Authors:
    • Zhenbo Geng
    • Lianbo Wei
    • Chunhua Zhang
    • Xiaohua Yan
  • View Affiliations

  • Published online on: May 22, 2017     https://doi.org/10.3892/etm.2017.4492
  • Pages: 91-96
  • Copyright: © Geng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to determine the effect of Astragalus polysaccharide (APS) in an in vivo and in vitro rat model of muscle atrophy (cachexia) caused by chronic renal failure (CRF), along with the potential corresponding roles of atroglin‑1 and the ubiquitin‑proteasome pathway. A rat model of CRF was established using subtotal bilateral nephrectomy. It was observed by reverse transcription‑quantitative polymerase chain reaction and western blot analysis that APS and the specific inhibitor of nuclear factor (NF)‑κB, pyrrolidine dithiocarbamate (PDTC), significantly reduced the expression of atrogin‑1, ubiquitin and the NF‑κB subunit p65 mRNA in rat skeletal muscle in vivo and in vitro, respectively (P<0.05). NF‑κB and PDTC also markedly reduced the expression of atrogin‑1, ubiquitin and p65 protein. In addition, cultured rat myoblasts pretreated with tumor necrosis factor (TNF)‑α exhibited significantly reduced expression of atrogin‑1, ubiquitin and p65 mRNA in vitro (P<0.05). Fluorescence microscopy was subsequently used to evaluate TNF‑α‑treated myoblasts administered with APS or PDTC, whereby no evidence of muscle cell atrophy was observed in cells treated with APS. These data suggest that APS may delay muscle cell atrophy associated with cachexia in CRF by targeting atrogin‑1 and the ubiquitin-proteasome pathway.
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July-2017
Volume 14 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Geng Z, Wei L, Zhang C and Yan X: Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway. Exp Ther Med 14: 91-96, 2017.
APA
Geng, Z., Wei, L., Zhang, C., & Yan, X. (2017). Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway. Experimental and Therapeutic Medicine, 14, 91-96. https://doi.org/10.3892/etm.2017.4492
MLA
Geng, Z., Wei, L., Zhang, C., Yan, X."Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway". Experimental and Therapeutic Medicine 14.1 (2017): 91-96.
Chicago
Geng, Z., Wei, L., Zhang, C., Yan, X."Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway". Experimental and Therapeutic Medicine 14, no. 1 (2017): 91-96. https://doi.org/10.3892/etm.2017.4492