https://www.sciencedirect.com/science/article/pii/S0014480019303582?via%3Dihub
https://www.ncbi.nlm.nih.gov/pubmed/31837326?dopt=Abstract
TITLE:
Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells.
DESCRIPTION:
Related Articles
Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells.
Exp Mol Pathol. 2020 02;112:104355
Authors: Dong Y, Yan X, Yang X, Yu C, Deng Y, Song X, Zhang L
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.
PMID: 31837326 [PubMed – indexed for MEDLINE]
PMID:
PubMed:31837326
DATE FOUND:
07/16/20 06:57AM
LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/31837326?dopt=Abstract
