RRC ID 58649
Author Dong Y, Yan X, Yang X, Yu C, Deng Y, Song X, Zhang L.
Title RETRACTED: Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells.
Journal Exp Mol Pathol
Abstract BACKGROUND:Notoginsenoside R1 (NG-R1) exhibits a pharmacological activity against excessive inflammation. Here, we aimed to ascertain the anti-inflammatory role of NG-R1 in ankylosing spondylitis (AS) as well as the possible mechanism which is still under to be elucidated.
METHODS:In this study, lipopolysaccharide (LPS) was applied to evoke extreme inflammation in ATDC5 cells. To investigate the anti-inflammatory property of NG-R1, ATDC5 cells were exposed to NG-R1 prior to LPS stimulation. microRNA-301a (miR-301a)-overexpressed ATDC5 cells were established which confirmed by qRT-PCR. Then, inflammatory lesions were indicated by cell viability, apoptosis and inflammatory factors, including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α). Nuclear factor-kappa B (NF-κB) pathway was determined by Western blotting assay.
RESULTS:We found NG-R1 dramatically dampened the decrease of cell viability, facilitation of apoptosis and abundance of inflammatory factors induced by LPS. Additionally, NG-R1 pre-incubation impeded LPS-induced accumulation of miR-301a. However, the protective capacity of NG-R1 was impaired by miR-301a overexpression. Of note, LPS-caused phosphorylation of p65 and inhibitor of nuclear factor kappa-B alpha (IκBα) was repressed by NG-R1, while further enhanced in miR-301-transfected ATDC5 cells.
CONCLUSION:NG-R1 relived LPS-elicited inflammatory damages via blocking NF-κB in a miR-301a-silenced manner.
Volume 112
Pages 104355
Published 2020-2-1
DOI 10.1016/j.yexmp.2019.104355
PII S0014-4800(19)30358-2
PMID 31837326
MeSH Animals Cell Survival / drug effects Cytokines / genetics Gene Expression Regulation / drug effects Ginsenosides / pharmacology* Humans Inflammation / chemically induced Inflammation / drug therapy* Inflammation / genetics Inflammation / pathology Lipopolysaccharides / toxicity Mice MicroRNAs / genetics* NF-kappa B / genetics Osteoarthritis / drug therapy Osteoarthritis / genetics Osteoarthritis / pathology Signal Transduction / drug effects Spondylitis, Ankylosing / chemically induced Spondylitis, Ankylosing / drug therapy* Spondylitis, Ankylosing / genetics Spondylitis, Ankylosing / pathology
IF 2.28
Times Cited 0
Human and Animal Cells ATDC5(RCB0565)