Buyang Huanwu Tang improves denervation-dependent muscle atrophy by increasing ANGPTL4, and increases NF-κB and MURF1 levels

Zhou,Lan; Huang,Yufang; Xie,Hui; Mei,Xiaoyun

doi:10.3892/mmr.2017.8306

Buyang Huanwu Tang improves denervation-dependent muscle atrophy by increasing ANGPTL4, and increases NF-κB and MURF1 levels

Authors:
- Lan Zhou
- Yufang Huang
- Hui Xie
- Xiaoyun Mei
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Affiliations: Basic Theory of Traditional Chinese Medicine Staff Room, Basic Medical College, Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China, Pathological Staff Room, Basic Medical College, Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China, Pharmacological Staff Room, School of Pharmacy, Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China
Published online on: December 19, 2017 https://doi.org/10.3892/mmr.2017.8306
Pages: 3674-3680
Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Denervated-dependent skeletal muscle atrophy (DSMA) is a disorder caused by the peripheral neuro‑disconnection of skeletal muscle. The current study aimed to investigate the molecular mechanism and potential therapeutic strategies for the DSMA. A DSMA rat model was established. A lentiviral vector expressing small interfering RNA (siRNA) targeting angiopoietin‑like protein 4 (ANGPTL4) was generated and injected into the rats that were also treated with Buyang Huanwu Tang (BYHWT). Reverse transcription‑quantitative polymerase chain reaction was performed to examine ANGPTL4 mRNA expression in anterior cervical muscle samples. Western blot assay was used to evaluate ANGPTL4, nuclear factor‑κB (NF‑κB) and muscle RING‑finger protein‑1 (MURF1) expression. The ultrastructure of muscle tissues was viewed using transmission electron microscopy. The cell apoptosis in muscle tissues was detected using the terminal deoxynucleotidyl transferase dUTP nick end labeling. The results indicated that BYHWT treatment increased ANGPTL4 mRNA and protein levels in muscle tissues. The suppression of ANGPTL4 using siRNA significantly increased inflammatory cells compared with the control siRNA group. BYHWT protected the ultrastructure muscle tissues and inhibited cell apoptosis in the DSMA model. The protective effect of BYHWT protected may be mediated by increased expression of NF‑κB p65 and MURF1. In conclusion, BYHWT may improve denervation‑dependent muscle atrophy by increasing ANGPTL4 expression, involving NF‑κB and MURF1 signaling.

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