Home 
General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.6, p. 521–529, 2023
General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.6, p. 521–529, 2023
Journal info
|
||
Select Journal
Journals
Bratislava Medical Journal Endocrine Regulations General Physiology and Biophysics 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 Neoplasma Acta Virologica Studia Psychologica Cardiology Letters Psychológia a patopsych. dieťaťa Kovove Materialy-Metallic Materials Slovenská hudbaWebshop Cart
Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.
General Physiology and Biophysics Vol.42, No.6, p. 521–529, 2023 |
||
| Title: Polydatin inhibited TNF-α-induced apoptosis of skeletal muscle cells through AKT-mediated p38 MAPK and NF-κB pathways | ||
| Author: Yongli Liu, Fang Xie, Changhuai Lu, Zongbo Zhou, Shudong Li, Jia Zhong, Qian Li, Xianfang Shao | ||
| Abstract: Skeletal muscle atrophy severely impacts one’s quality of life. The effects and mechanism of polydatin on skeletal muscle atrophy are unclear. This study investigated the effects and mechanism of polydatin on TNF-α-induced skeletal muscle cells. The skeletal muscle cell atrophy model was established by inducing C2C12 cells with TNF-α. Cell viability, IL-1β levels and cell apoptosis were assessed. The mRNA and protein expression levels of apoptosis-related proteins were measured. Meanwhile, the binding of polydatin to AKT was analyzed by molecular docking. TNF-α reduced cell fusion and viability while up-regulated IL-1β level and promoted cell apoptosis. TNF-α activated AKT, NF-κB, and p38 MAPK signaling pathways. Polydatin reversed these effects induced by TNF-α, with a low concentration being more effective. Polydatin was predicted to bind to GLY162, PHE161, GLU198, THR195 and GLU191 sites of AKT protein through van der Waals force and conventional hydrogen bonds. Overexpression of AKT led to increased phosphorylation levels of AKT, p38, and p65 proteins, as well as IL-1β levels and cell apoptosis. Polydatin inhibited TNF-α-induced apoptosis of C2C12 cells by regulating NF-κB and p38 MAPK signaling pathways through AKT. This suggests that polydatin shows promise as a new drug for the treatment of skeletal muscle atrophy. |
||
| Keywords: Polydatin — p38 MAPK — NF-κB — AKT | ||
| Published online: 14-Nov-2023 | ||
| Year: 2023, Volume: 42, Issue: 6 | Page From: 521, Page To: 529 | |
| doi:10.4149/gpb_2023027 |
||
|
|
 download file |
|