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Physcion 8Oβglucopyranoside extracted from Polygonum cuspidatum exhibits antiproliferative and antiinflammatory effects on MH7A rheumatoid arthritisderived fibroblastlike synoviocytes through the TGFβ/MAPK pathway

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The present study aimed to investigate the antiarthritic effect of physcion 8Oβglucopyranoside (POGD) and its possible mechanisms. The antiproliferative effects of POGD on MH7A cells were detected using a CCK8 assay, and the release of proinflammatory cytokines, interleukin (IL)1β, IL6, IL8, IL12 and IL17A, were determined by ELISA. A type II collageninduced arthritis (CIA) rat model was established to evaluate the antiarthritic effect of POGD in vivo. The paw volumes, arthritis indices and serum levels of tumor necrosis factor (TNF)α, IL1β, IL6, IL8, IL17A were determined by ELISA. The mRNA expression levels of matrix metalloproteinase (MMP)2, MMP3, MMP9, vascular endothelial growth factor and cyclooxygenase2 were determined by reverse transcriptionquantitative polymerase chain reaction analysis, and the expression levels of transforming growth factor (TGF)β1, small mothers against decapentaplegic (Smad)4, Smad7, cJun Nterminal kinase (JNK), phosphorylated (p)JNK, pP38, P38, pextracellular signalregulated kinase (ERK)1/2, ERK1/2, nuclear factor (NF)κB p65 in the nucleus (N), cytosolic NFκB p65 (C), and inhibitor of NFκB (IκB) were determined by western blot analysis. The results indicated that POGD significantly inhibited MH7A cell growth. POGD markedly inhibited paw swelling and the arthritis indices of the CIA rats, and POGD may also inhibit the release of proinflammatory cytokines. Furthermore, POGD downregulated the expression levels of TGFβ1, Smad4, NFκB p65 (N), p38, pp38, pERK1/2, JNK, pJNK, TGFβ1, Smad4, pJNK, JNK, pP38, P38, pERK1/2, ERK1/2 and NFκB p65 (N), and upregulated the Smad7, NFκB p65 (C) and IκB in TNFα induced MH7A cells. In conclusion, the results suggested that POGD is a promising potential antiinflammatory drug, and that POGD may decrease the expression of proinflammatory cytokines and mediators via inhibiting the TGFβ/NFκB/mitogenactivated protein kinase pathways.
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Document Type: Research Article

Affiliations: 1: Department of Rheumatology, Shandong Zibo Central Hospital, Zibo, Shandong 255036, P.R. China 2: Dezhou People's Hospital, Department of Traditional Chinese Medicine Rheumatology, Dezhou, Shandong 253000, P.R. China

Publication date: January 1, 2018

More about this publication?
  • The International Journal of Molecular Medicine is a monthly, peer-reviewed journal devoted to the publication of high quality studies related to the molecular mechanisms of human disease. The journal welcomes research on all aspects of molecular and clinical research, ranging from biochemistry to immunology, pathology, genetics, human genomics, microbiology, molecular pathogenesis, molecular cardiology, molecular surgery and molecular psychology.

    The International Journal of Molecular Medicine aims to provide an insight for researchers within the community in regard to developing molecular tools and identifying molecular targets for the diagnosis and treatment of a diverse number of human diseases.
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