Anti-proliferation and anti-inflammation effects of corilagin in rheumatoid arthritis by downregulating NF-κB and MAPK signaling pathways

Shen, Yue; Teng, Li; Qu, Yuhan; Liu, Jie; Zhu, Xudong; Chen, Shan; Yang, Longfei; Huang, Yuehui; Qin, Song; Fu, Qiang

doi:10.1016/j.jep.2021.114791

Cited by 46 publications

(21 citation statements)

References 43 publications

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“…Plausibly, products from hydrolysis and metabolism, such as GA, EA, and UroA, participate in the biological effect, although their formation at the gut level has rarely been addressed. This evidence is supported by several in vivo experiments, in which HTs and metabolites were administered as individual compounds through the oral route at comparable doses: EA (50 mg/kg) ameliorated the inflammatory profile in RA models [ 31 , 32 , 33 , 34 , 35 ]; similarly EA, GA, and UroA (10–20 mg/kg) inhibited gut inflammation in IBD models [ 64 , 65 , 66 , 70 , 71 , 72 ], while EA (10 mg/kg) and GA (20–80 mg/kg) reduced allergic inflammation in AD, asthma, and rhinitis [ 86 , 88 , 96 , 102 ]. Remarkably, HTs have frequently been mentioned for direct antibacterial and antiviral activity [ 106 ], which may suggest a restrained impact on infection risk.…”

Section: Discussionmentioning

confidence: 69%

“…The in vivo results showed that corilagin significantly reduced paw swelling and arthritis score and inhibited joint erosion and the infiltration of inflammatory cells; pro-inflammatory cytokines were also inhibited at the serum level (IL-6, TNF-α, IL-1β, and IL-17). In fibroblast-like synoviocyte (FLS) cells challenged by IL-1β, corilagin (6.25 or 12.5 μM) impaired COX-2, iNOS, and MMPs expression through MAPKs and NF-κB inhibition [ 32 ].…”

Section: Resultsmentioning

confidence: 99%

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Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases

et al. 2022

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Plants rich in hydrolyzable tannins were traditionally used all over the world for a variety of chronic inflammatory disorders, including arthritis, colitis, and dermatitis. However, the knowledge of their immunological targets is still limited though fundamental for their rational use in phytotherapy. The recent advances regarding the pathogenesis of inflammatory-based diseases represent an opportunity to elucidate the pharmacological mechanism of plant-derived metabolites with immunomodulatory activity. This review collects recent articles regarding the role of hydrolyzable tannins and their gut metabolites in Th1, Th2, and Th17 inflammatory responses. In line with the traditional use, rheumatoid arthritis (RA), inflammatory bowel diseases (IBDs), psoriasis, atopic dermatitis (AD), and asthma were the most investigated diseases. A substantial body of in vivo studies suggests that, beside innate response, hydrolyzable tannins may reduce the levels of Th-derived cytokines, including IFN-γ, IL-17, and IL-4, following oral administration. The mode of action is multitarget and may involve the impairment of inflammatory transcription factors (NF-κB, NFAT, STAT), enzymes (MAPKs, COX-2, iNOS), and ion channels. However, their potential impact on pathways with renewed interest for inflammation, such as JAK/STAT, or the modulation of the gut microbiota demands dedicate studies.

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Section: Discussionmentioning

confidence: 69%

Section: Resultsmentioning

confidence: 99%

Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases

et al. 2022

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“…The Mitogen-activated protein kinase kinase (MEK)/ Extracellular signal-regulated kinase (ERK) signaling cascades are important for inflammatory progression in RA (32,33). We, therefore, sought to determine whether Antcin K affects MEK and ERK signaling.…”

Section: Antcin K Inhibits Vcam-1 Synthesis By Suppressing Mek1/2-erk...mentioning

confidence: 99%

“…4b-e and 5be). The p38 signaling pathway is involved in the regulation of CAM and proinflammatory cytokine expression during RA development (33,34). We, therefore, investigated whether Antcin K inhibits VCAM-1 expression and monocyte adhesion in RASFs via the p38 signaling pathway.…”

Section: Antcin K Inhibits Vcam-1 Synthesis By Suppressing Mek1/2-erk...mentioning

confidence: 99%

Antcin K inhibits VCAM-1-dependent monocyte adhesion in human rheumatoid arthritis synovial fibroblasts

Achudhan¹,

Chang²,

Liu³

et al. 2022

Food & Nutrition Research

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Background: Antcin K, an extract of Antrodia cinnamomea (a medicinal mushroom endemic to Taiwan commonly used in Chinese medicine preparations), inhibits proinflammatory cytokine production and angiogenesis in human rheumatoid arthritis synovial fibroblasts (RASFs), major players in RA disease. Antcin K also inhibits disease activity in mice with collagen-induced arthritis (CIA). Up until now, the effects of Antcin K upon cell adhesion molecules (CAMs) were unknown. Methods: RA and healthy synovial tissue samples (n = 10 in each group) were retrieved from the Gene Expression Omnibus (GEO) database (accession code: GDS5401) to compare CAM and monocyte marker expressions. In addition, synovial tissue samples from six RA patients and six patients undergoing arthroscopy for trauma/joint derangement (healthy controls) were subjected to immunohistochemical (IHC) analysis. mRNA and protein expression levels were analyzed in RASFs using RT-qPCR (Reverse transcription-quantitative polymerase chain reaction) and Western blot. RASFs were incubated with Antcin K and examined for monocyte adherence by fluorescence microscopy. Ankle joint tissue specimens from a CIA mouse model and healthy controls were stained with hematoxylin and eosin (H&E) and Safranin-O/Fast Green to examine histological changes and evidence of bone loss. IHC analysis determined levels of vascular cell adhesion molecule 1 (VCAM-1) and CD11b in CIA ankle tissue and clinical synovial tissue. Results: Levels of VCAM-1 expression were higher in the GEO database specimens and the study’s clinical samples of RA synovial tissue compared with the healthy specimens. Antcin K dose-dependently inhibited VCAM-1 expression and monocyte adhesion in RASFs. Antcin K also significantly inhibited levels of VCAM-1 and monocyte CD11b expression in CIA tissue. These effects appeared to be mediated by MEK1/2-ERK, p38, and AP-1 signaling. Conclusions: Antcin K seems promising for the treatment of RA and deserves further investigations.

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“…TNF-α triggers NF-κB activation by a variety of signaling molecules, including TRAF2 (TNF receptor-associated factor 2), RIP (receptor-interacting protein), and the IKK (IκB kinase) complex. Another signal pathway activated by TNF-α is mitogen-activated protein kinase pathways (including p38, JNK, and ERK1/2), which has been strongly associated with many of the processes that mediate the pathological features of RA [7]. The p38 MAPK and JNK (Jun N-terminal kinase) pathway inhibitors attract more attention since they can reduce both the synthesis of proinflammatory cytokine and their intracellular signaling [8].…”

Section: Introductionmentioning

confidence: 99%

Ebosin Attenuates the Inflammatory Responses Induced by TNF-α through Inhibiting NF-κB and MAPK Pathways in Rat Fibroblast-Like Synoviocytes

Zhang

Wang

Bai

et al. 2022

Journal of Immunology Research

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Tumor necrosis factor-α (TNF-α) lies at the apex of signal transduction cascades that results in induced destruction of joints in rheumatoid arthritis. It is therefore of great medicinal interest to modulate the cellular responses to TNF-α. Ebosin, a novel exopolysaccharide derived from Streptomyces sp, has been demonstrated to have remarkable therapeutic actions on collagen-induced arthritis in rats, while it also suppressed the production of IL-1β, TNF-α, and IL-6 at both mRNA and protein levels in cultured fibroblast-like synoviocytes. In order to further understand the potential mechanisms involved in the anti-inflammatory effects of ebosin at molecular level, we investigated the impact of it on the activation of MAPK and NF-κB pathways following TNF-α induced in fibroblast-like synoviocytes (FLS). The results showed that the phosphorylation levels of TNF-α-induced p38, JNK1, JNK2, IKKα, IKKβ, and IκB, as well as NF-κB nuclear translocation, were reduced significantly in FLS cells in response to ebosin. Furthermore, we proved that ebosin decreased the level of NF-κB in the nucleus and blocked the DNA-binding ability of NF-κB using electrophoresis mobility gel shift assay. Besides, low levels of matrix metalloproteinases (MMP-1 and MMP-3) and chemokines (interleukin-8 and RANTES) were found in TNF-α-stimulated fibroblast-like synoviocytes treated with ebosin. These results indicate that ebosin can suppress a range of activities in both MAPK and NF-κB pathways induced by TNF-α in rat fibroblast-like synoviocytes, which provides a rationale for examining the use of ebosin as a potential therapeutic candidate for rheumatic arthritis.

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Anti-proliferation and anti-inflammation effects of corilagin in rheumatoid arthritis by downregulating NF-κB and MAPK signaling pathways

Cited by 46 publications

References 43 publications

Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases

Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases

Antcin K inhibits VCAM-1-dependent monocyte adhesion in human rheumatoid arthritis synovial fibroblasts

Ebosin Attenuates the Inflammatory Responses Induced by TNF-α through Inhibiting NF-κB and MAPK Pathways in Rat Fibroblast-Like Synoviocytes

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