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Inflammation

, Volume 42, Issue 2, pp 506–515 | Cite as

Compound GDC, an Isocoumarin Glycoside, Protects against LPS-Induced Inflammation and Potential Mechanisms In Vitro

  • Yuqin Zhang
  • Guohong Yan
  • Chengtao Sun
  • Lihong Nan
  • Xiaoying Wang
  • Wei XuEmail author
  • Kedan ChuEmail author
ORIGINAL ARTICLE

Abstract

Compound 3R-(4′-hydroxyl-3′-O-β-D-glucopyranosyl phenyl)-dihydro isocoumarin (GDC) is a natural isocoumarin, recently isolated from the stems of H. paniculiflorum. However, we know little about the effects of GDC on rheumatoid arthritis (RA). This study aims to investigate the protective effects and potential mechanisms of GDC against LPS-induced inflammation in vitro. Fibroblast-like synoviocytes (FLSs) obtained from synovial tissue of rats were induced by lipopolysaccharide (LPS) and treated with GDC. Cell viability was determined by mitochondrial-respiration-dependent3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay. Secretion of various inflammatory mediators was analyzed by ELISA and RayBio® Rat Cytokine Antibody Array. Potential mechanisms that are associated with anti-inflammatory effect were examined by Western blot. Results showed that GDC significantly inhibited the production of tumor necrosis factor alpha (TNF-α) and interleukin- (IL-) 6 induced by LPS. GDC also reduced the expression of inducible nitric oxide synthase (iNOS), TNF-α, IL-6, and IL-1β, as well as proinflammatory cytokines such as activin A, ciliary neurotrophic factor (CNTF), fractalkine, IFN-γ, IL-4, and TIMP-1. Moreover, GDC inhibited LPS-induced phosphorylation of extracellular regulated protein kinases (ERK1/2), p38 mitogen-activated protein kinases (p38), c-Jun N-terminal kinase (JNK), and IκB. And GDC also blocked NF-κBp65 nuclear translocation. All the results suggested that the protective effects of GDC against LPS-induced inflammation in vitro may be related with NF-κB and JNK signaling pathway.

KEY WORDS

rheumatoid arthritis isocoumarin fibroblast-like synoviocyte inflammation NF-κB signaling pathway MAPK signaling pathway 

Notes

Funding Information

The project was financially supported by Key Laboratory of Tropical Medicinal Plant Chemistry of Ministry of Education of Hainan Normal University, the National Natural Science Foundation of China (NO.81370096), and Fujian Provincial Department of Education to Support Provincial University Special Project (No. JK2017023).

Compliance with Ethical Standards

Conflict of Interests

The authors declare that they have no conflicts of interest.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Pharmacy College of Fujian University of Traditional Chinese MedicineFuzhouPeople’s Republic of China
  2. 2.Key Laboratory of Tropical Medicinal Plant Chemistry of Ministry of EducationHainan Normal UniversityHaikouPeople’s Republic of China
  3. 3.State Key Laboratory of Chinese Pharmacies of Fujian Provincial Department of Science and Technology of Fujian University of Traditional Chinese MedicineFuzhouPeople’s Republic of China
  4. 4.People’s Hospital Affiliated to Fujian University of Traditional Chinese MedicineFuzhouPeople’s Republic of China

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