Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells.

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. 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. 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. NG-R1 relived LPS-elicited inflammatory damages via blocking NF-κB in a miR-301a-silenced manner. • Notoginsenoside R1 protects ATDC5 cells from inflammation-caused lesions; • Lipopolysaccharide-induced miR-301a is eliminated by notoginsenoside R1; • miR-301a-mediated blockade of NF-κB pathway is triggered by notoginsenoside R1. [ABSTRACT FROM AUTHOR]