Ellagic acid protects type II collagen induced arthritis in rat via diminution of IKB phosphorylation and suppression IKB-NF-kB complex activation: in vivo and in silico study
5
Issued Date
2022-10-01
Resource Type
ISSN
09254692
eISSN
15685608
Scopus ID
2-s2.0-85135686283
Pubmed ID
35939220
Journal Title
Inflammopharmacology
Volume
30
Issue
5
Start Page
1729
End Page
1743
Rights Holder(s)
SCOPUS
Bibliographic Citation
Inflammopharmacology Vol.30 No.5 (2022) , 1729-1743
Suggested Citation
Khan M.A., Rabbani G., Kumari M., Khan M.J. Ellagic acid protects type II collagen induced arthritis in rat via diminution of IKB phosphorylation and suppression IKB-NF-kB complex activation: in vivo and in silico study. Inflammopharmacology Vol.30 No.5 (2022) , 1729-1743. 1743. doi:10.1007/s10787-022-01022-x Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/84900
Title
Ellagic acid protects type II collagen induced arthritis in rat via diminution of IKB phosphorylation and suppression IKB-NF-kB complex activation: in vivo and in silico study
Author(s)
Other Contributor(s)
Abstract
Objective: The present study was designed to explore the potential anti-inflammatory and anti-arthritic effects of ellagic acid (EA) in collagen-induced arthritis (CIA). Methods: CIA rats were treated with MTX (0.25 mg/kg body wt.) and EA (50 mg/kg b.wt.) for a period of 20 days. The effects of treatment in the rats were assessed biochemically by analyzing inflammatory mediators (NF-kB, iNOS, TNF-α, IL-1β, IL-6 and IL-10) and oxidative stress related parameters (MPO, NO, LPO, catalase, SOD, GSH). In addition, we also assessed the expression of some inflammatory mediators TNF-α, CD8 + though immunohistochemistry in the joint tissue. Results: In the present study, we found expression and synthesis of transcription factor NF-kB was prominent in CIA rats. In addition, main pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6, and the anti-inflammatory IL-10, was also stand out. Further, reactive oxygen/nitrogen species was also elevated in CIA rats. Treatment with EA ameliorates all the above mentioned inflammatory and oxidative stress related parameters to near normal. Further, we also confirmed the expression of TNF-α, CD8+ T cells through immunohistochemistry was mitigates in joint tissue of EA treated rats. We find EA significantly inhibited the developmental phase of arthritis. Conclusion: These results suggest that EA act as potent anti-arthritic and anti-inflammatory agent that could be used as a tool for the development of new drug for the treatment of arthritis. Graphical abstract: [Figure not available: see fulltext.]