Reference - Detail
RRC ID | 58649 |
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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 |
Resource | |
Human and Animal Cells | ATDC5(RCB0565) |