Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells (Retracted article. See vol. 126, 2022)
Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells (Retracted article. See vol. 126, 2022)
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DOI：
10.1016/j.yexmp.2019.104355
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发表时间：
2020-02-01
影响因子：
3.6
通讯作者：
Zhang, Lei
中科院分区：
文献类型：
--
作者：
Dong, Yan;Yan, Xia;Zhang, Lei
背景：三七皂苷R1（NG-R1）具有抗过度炎症的药理活性。本研究旨在探讨NG-R1在强直性脊柱炎（ankylosing spondylitis，AS）中的抗炎作用及其可能机制。方法：采用脂多糖（lipopolysaccharide，LPS）诱导ATDC 5细胞的极端炎症反应。为了研究NG-R1的抗炎特性，在LPS刺激之前将ATDC 5细胞暴露于NG-R1。建立microRNA-301 a（miR-301 a）过表达的ATDC 5细胞，其通过qRT-PCR证实。然后，通过细胞活力、凋亡和炎性因子（包括白细胞介素-1 β（IL-1 β）、IL-6和肿瘤坏死因子-α（TNF-α））指示炎性病变。结果：NG-R1可明显抑制LPS诱导的细胞存活率下降，促进细胞凋亡，增加炎症因子的表达。此外，NG-R1预孵育阻碍了LPS诱导的miR-301 a积累。然而，NG-R1的保护能力受到miR-301 a过表达的损害。结论：NG-R1通过抑制miR-301 a沉默NF-κ B，减轻LPS诱导的炎症损伤。
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-1 beta), IL-6 and tumor necrosis factor-alpha (TNF-alpha). Nuclear factor-kappa B (NF-kappa B) 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 (I kappa B alpha) 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-kappa B in a miR-301a-silenced manner.