Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice.

doi:10.1093/rheumatology/ket178

Paper

Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice.

Published Sep 1, 2013 · J. Hwang, E. Noh, Sunhee Moon

Rheumatology

Q1 SJR score

79

Citations

2

Influential Citations

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Abstract

OBJECTIVE Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is one of the active components present in the root and rhizome of Rheum palmatum. It has been shown to contain biological activity (antitumour, antibacterial, diuretic and vasorelaxant effects). However, the mechanisms underlying the anti-arthritic effect of emodin have not been elucidated. Here we investigated whether emodin treatment would modulate the severity of the disease in an experimental arthritis model. METHODS We evaluated the effects of emodin on CIA mice in vivo. RESULTS The pathological processes of RA are mediated by a number of cytokines and MMPs. Expression of these proinflammatory mediators is controlled by nuclear factor-κB (NF-κB). This study was performed to explore the effect of emodin on control of the NF-κB activation pathway and to investigate whether emodin has anti-inflammatory effects in CIA mice in vivo. Emodin inhibited the nuclear translocation and DNA binding of NF-κB subunits, which were correlated with its inhibitory effect on cytoplasmic IκBα degradation in CIA mice. These events further suppressed chemokine production and MMP expression. In addition, emodin inhibited the osteoclast differentiation induced by M-CSF and receptor activation of NF-κB ligand in bone marrow macrophages. CONCLUSION These findings suggest that emodin exerts anti-inflammatory effects in CIA mice through inhibition of the NF-κB pathway and therefore may have therapeutic value for the treatment of RA.

Non-RCT

Animal Study

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Highly Cited

Study Snapshot

Emodin, a component in Rheum palmatum, exhibits anti-inflammatory effects in mice by inhibiting the NF-B pathway, suggesting potential therapeutic value for treating RA.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice.

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References

Citations

Triterpenoids from the leaves of Eleutherococcus sessiliflorus, and their antiproliferative activities in TNF-α induced HFLS-RA cells.

Elesesterpene M, chiisanogenin, chiisanoside, and 3-methylisochiisanoside significantly inhibit TNF--induced proliferation of HFLS-RA cells in vitro.

Emodin promotes the recovery of rheumatoid arthritis by regulating the crosstalk between macrophage subsets and synovial fibroblast subsets

Emodin promotes rheumatoid arthritis recovery by regulating macrophage subsets and exosome secretion, affecting inflammatory factors in synovial fibroblasts, and showing good therapeutic efficacy in RA patients.

Emodin ameliorates matrix degradation and apoptosis in nucleus pulposus cells and attenuates intervertebral disc degeneration through LRP1 in vitro and in vivo.

Emodin effectively alleviates intervertebral disc degeneration by inhibiting ECM degradation and apoptosis through the inhibition of NF-B via LRP1.

Water extracts of Polygonum Multiflorum Thunb. and its active component emodin relieves osteoarthritis by regulating cholesterol metabolism and suppressing chondrocyte inflammation

Polygonum multiflorum Thunb. (PMT) water extract, with its active component emodin, effectively improves osteoarthritis by regulating cholesterol metabolism and suppressing chondrocyte inflammation.

Epimedii Herba: An ancient Chinese herbal medicine in the prevention and treatment of rheumatoid arthritis

Epimedii Herba, a traditional Chinese medicine, shows promising curative effects against rheumatoid arthritis due to its multifunctional traits, including anti-inflammatory, immunoregulatory, cartilage and bone protective, antiangiogenic, and antioxidant activities.