FM0807 decelerates experimental arthritis progression by inhibiting inflammatory responses and joint destruction via modulating NF-κB and MAPK pathways

Zhang, Nanwen; Liu, Zhiwei; Luo, Huimin; Wu, Weifang; Nie, Kaimei; Cai, Lin; Tan, Shuangyu; Chen, Xiaole; Huang, Ying; Liu, Jiaxing; Lv, Meina; Zhang, Xin; Fan, Yun; Lin, Yu-Ying; Ye, Shennan; Liu, Yang; Wu, Lixian; Xu, Jianhua

doi:10.1042/bsr20182263

Cited by 11 publications

(13 citation statements)

References 43 publications

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“…57 Okamoto et al 72 of the included studies. 47,48,53,64,68,69,70,75,77,78,80 However, Khayyal et al 63 did not detect a significant decrease in serum levels of TNFα, IL-6 and CRP with 5 mg/kg curcumin. Likewise, Fan et al 56 detected no significant decrease in the serum levels of TNFα, IL-1 and IL-6.…”

Section: Curcumin Effect On Inflammatory Markers and Matrix Metalloproteinasesmentioning

confidence: 95%

“…(n = 6) 57,68,69,72,75,78 ; and Balb/c (n = 1) 58 ) or rats (Wistar (n = 1 9) 47,49,51,52,53,54,55,56,60,62,63,64,65,66,67,70,71,82,83 ; Sprague-Dawley (n = 9) 48,50,61,74,76,77,79,80,81 ; Charles Foster (n = 1) 73 and in one study there was no information about the kind of rats 59 ). The induction of RA was performed by injection of complete Freund's adjuvant (CFA) (n = 19), 47,48,49,50,51,52,54,55,63,64,65,66,67,70,73,…”

Section: Study Characteristicsmentioning

confidence: 99%

“…The risk of bias assessment and tier classifications of in vivo studies have been presented in TableS4. Sixteen of the 37 in vivo studies used randomization for allocating animals in different experimental groups 47,51,56,58,61,63,65,66,70,74,75,76,77,80,81,83. The blindness of outcome assessors to the treatment groups was mentioned in eight studies 47,54,57,61,68,69,79,80.…”

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confidence: 99%

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Curcumin and rheumatoid arthritis: A systematic review of literature

2021

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Background: Curcumin is a natural polyphenol and the main compound from the rhizome of Turmeric (Curcuma longa) and other Curcuma species. It has been widely used for different medical purposes, such as improvement of pain and inflammatory conditions in various diseases.Purpose: This systematic review was aimed to assess all studies regarding the efficacy of the pure form of curcumin (unformulated curcumin) on rheumatoid arthritis (RA). Methods: The comprehensive search of the literature was done until September 2020 on the MEDLINE, Embase, Scopus and Web of Knowledge databases. Out of 2079 initial records, 51 articles (13 in vitro and 37 animal and one human) were met our inclusion criteria. Results: Most studies have shown the curative effects of curcumin on clinical and inflammatory parameters of RA and reported different mechanisms; inhibition of mitogen-activated protein kinase family, extracellular signal-regulated protein kinase, activator protein-1 and nuclear factor kappa B are the main mechanisms associated with the anti-inflammatory function of curcumin in RA. The results of the only human study showed that curcumin significantly improved morning stiffness, walking time and joint swelling. Conclusion:In conclusion, curcumin seems to be useful, and it is recommended that more human studies be performed to approve the cellular and animal results and determine the effective and optimal doses of curcumin on RA patients. Review criteria• The MEDLINE database (PubMed), Embase, Scopus, and Thomson Reuters Web of Knowledge were systematically and comprehensively searched until September 2020, using related keywords.• All English written original in vitro, animal, and human studies on the effects of curcumin on RA were included.

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Section: Curcumin Effect On Inflammatory Markers and Matrix Metalloproteinasesmentioning

confidence: 95%

Section: Study Characteristicsmentioning

confidence: 99%

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confidence: 99%

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Curcumin and rheumatoid arthritis: A systematic review of literature

2021

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“…NF-κB signaling is closely associated with inflammatory cell infiltration (42)(43)(44). On the basis of the underlying mechanism, phosphorylation of NF-κB (p65) and downregulation of IκBα may activate NF-κB signaling (45).…”

Section: Discussionmentioning

confidence: 99%

microRNA‑23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12

et al. 2021

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Rheumatoid arthritis (RA) is a common systemic, inflammatory and autoimmune disorder. MicroRNAs (miRs) are strongly associated with the initiation and progression of RA. However, the functions and mechanisms underlying miR-23 in RA are not completely understood. Therefore, the present study aimed to investigate the molecular mechanisms underlying miR-23 in RA. A bioinformatics tool (StarBase) and a wide range of experimental assays, including reverse transcription-quantitative PCR, western blotting, luciferase reporter assays and ELISAs, were performed to investigate the biological role of miR-23 in RA. The results indicated that miR-23 was downregulated and chemokine C-X-C motif ligand 12 (CXCL12) was upregulated in RA samples compared with healthy samples. Furthermore, miR-23 overexpression suppressed inflammation via reducing TNF-α, IL-1β and IL-8 expression levels compared with the NC mimic group. Regarding the underlying mechanism, compared with NC mimic, miR-23 mimic decreased CXCL12 mRNA expression by binding to its 3'-untranslated region. Additionally, CXCL12 overexpression reversed miR-23 mimic-mediated effects on inflammation. NF-κB signaling is associated with inflammation. Therefore, the present study indicated that CXCL12 promoted inflammation by activating NF-κB signaling. In conclusion, miR-23 inhibited inflammation to alleviate RA by regulating CXCL12 via the NF-κB signaling pathway, which may serve as a potential target for the diagnosis and treatment of RA.

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“…The proliferating mass of fibroblast-like synoviocytes (FLS) locally invades the articular cartilage and bones and eventually destroys the whole joint. It causes excessive morbidity, mortality, and enormous socioeconomic burdens with an estimated prevalence of 0.5%-1% [1,2]. Proinflammatory factors secreted by immune cells increase activation, hyperproliferation, and cytokine secretions of RA FLS, and this increase is associated with the severity of articular cartilage degradation [3].…”

Section: Introductionmentioning

confidence: 99%

CypB-CD147 Signaling Is Involved in Crosstalk between Cartilage and FLS in Collagen-Induced Arthritis

Wang

Fan

et al. 2020

Mediators of Inflammation

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To investigate the crosstalk between cartilage and fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA), we adopted an in vitro coculture system model of collagen-induced arthritis (CIA) cartilage and CIA FLS monolayer. CIA rat samples of the synovium and femur head were collected for isolation of FLS and coculture system. Cartilages were treated with vehicle (Ctrl group), 10 ng/mL interleukin- (IL-) 1α (IL-1α group), and 10 ng/mL IL-1α plus 10 μM dexamethasone (Dex group) for 3 days before coculture with FLS for further 2 days. After the coculture, FLS were collected to determine the influences of articular cartilage on synoviocytes. Whether the CypB-CD147 signaling pathway is involved in the interactions between cartilage and FLS is assayed. Results showed that IL-1α-stimulated CIA cartilage promoted the proliferation and reduced the apoptosis of FLS. Increased inflammatory cytokines and decreased p57 expression were found in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. Upregulation of NF-κB and I-κB kinase β (IKK-β) and downregulation of the inhibitor of NF-κBα (I-κBα) protein were observed in cocultured FLS. After coculture, significant increases in the expression of cyclophilin B (CypB) and CD147 were observed in CIA cartilage and FLS, respectively. Furthermore, results of immunofluorescence staining showed that the anti-CD147 antibody significantly suppressed p65 nuclear translocation in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. In conclusion, inflammatory effects in the cartilage-FLS coculture system are associated with the CypB-CD147 mediating NF-κB pathway which may further enhance the inflammation in RA.

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FM0807 decelerates experimental arthritis progression by inhibiting inflammatory responses and joint destruction via modulating NF-κB and MAPK pathways

Cited by 11 publications

References 43 publications

Curcumin and rheumatoid arthritis: A systematic review of literature

Curcumin and rheumatoid arthritis: A systematic review of literature

microRNA‑23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12

CypB-CD147 Signaling Is Involved in Crosstalk between Cartilage and FLS in Collagen-Induced Arthritis

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