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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
- Source :
- Inflammopharmacology. 30:1729-1743
- Publication Year :
- 2022
- Publisher :
- Springer Science and Business Media LLC, 2022.
-
Abstract
- The present study was designed to explore the potential anti-inflammatory and anti-arthritic effects of ellagic acid (EA) in collagen-induced arthritis (CIA).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.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, CD8These 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.
- Subjects :
- Pharmacology
Interleukin-6
Nitrogen
Superoxide Dismutase
Tumor Necrosis Factor-alpha
Immunology
Anti-Inflammatory Agents
NF-kappa B
CD8-Positive T-Lymphocytes
Catalase
Arthritis, Experimental
Interleukin-10
Rats
Oxygen
Ellagic Acid
Animals
Cytokines
Pharmacology (medical)
Inflammation Mediators
Phosphorylation
Rats, Wistar
Subjects
Details
- ISSN :
- 15685608 and 09254692
- Volume :
- 30
- Database :
- OpenAIRE
- Journal :
- Inflammopharmacology
- Accession number :
- edsair.doi.dedup.....307180264c37ad3e604c1758e48f78c7