KMID : 0352720210450040510
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Journal of Ginseng Research 2021 Volume.45 No. 4 p.510 ~ p.518
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Inhibitory activity of gintonin on inflammation in human IL-1¥â-stimulated fibroblast-like synoviocytes and collagen-induced arthritis in mice
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Kim Mi-Jin
Sur Bong-Jun Villa Thea Nah Seung-Yeol Oh Sei-Kwan
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Abstract
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Background: Gintonin is a newly derived glycolipoprotein from the roots of ginseng. The purpose of this study is to investigate the anti-arthritic efficacy of Gintonin on various proteases and inflammatory mediators that have an important role in arthritis.
Methods: Fibroblast-like synoviocytes (FLS) were treated with Gintonin and stimulated with interleukin (IL)-1¥â 1 hour later. The antioxidant effect of Gintonin was measured using MitoSOX and H2DCFDA experiments. The anti-arthritic efficacy of Gintonin was examined by analyzing the expression levels of inflammatory mediators using RT-PCR, western blot, and ELISA. The phosphorylation of mitogen-activated protein kinase (MAPK) pathways and translocation of nuclear factor kappa B (NF-¥êB)/p65 into the nucleus were also analyzed using western blot, ELISA, and immunocytochemistry. Collagen-induced arthritis (CIA) mice model was used. Mice were orally administered with Gintonin (25, 50, and 100 mg/kg) every 2 days for 45 days. The body weight, arthritis score, squeaking score, and paw volume were measured as the behavioral parameters. After sacrifice, H&E and safranin-O staining were performed for histological analysis.
Results: Gintonin significantly inhibited the expression of inflammatory intermediates. Gintonin prevented NF-¥êB/p65 from moving into the nucleus through the JNK and ERK MAPK phosphorylation in FLS cells. Moreover, Gintonin suppressed the symptoms of arthritis in the CIA mice model.
Conclusion: As a result, the antioxidant and anti-inflammatory effects of Gintonin were demonstrated, and ultimately the anti-arthritic effect was proved. Collectively, Gintonin has a great potential as a therapeutic agent for arthritis treatment.
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KEYWORD
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gintonin, arthritis, inflammation, collagen-induced arthritis, cytokines
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