Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
Advanced search 
Year : 2020  |  Volume : 16  |  Issue : 72  |  Page : 803-811

Juglanin attenuated adjuvant-induced arthritis via inactivating NF-κB/IκBα and a disintegrin-like and metalloproteinase domain with thrombospondin-1 repeat pathways in experimental rats

1 College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China
2 Institute for Communicable Disease Control and Prevention of Shaanxi Provincial Centre for Disease Control and Prevention, Xi'an, Shaanxi Province, China
3 Reproductive Medicine Center, Tangdu Hospital, Fourth Military Medical University, Xinsi Road, Baqiao District, Xi'an, Shaanxi Province, China
4 Clinical Experimental Centre, Xi'an International Medical Center Hospital, Xitai Road, High-tech Zone, Xi'an, Shaanxi Province, China

Correspondence Address:
Lei Yan
Clinical Experimental Centre, Xi'an International Medical Center Hospital, No.777 Xitai Road, High-tech Zone, Xi'an, Shaanxi Province, 710100
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_106_20

Rights and Permissions

Background: Rheumatoid arthritis (RA) is an autoimmune and inflammatory disease affecting multiple joints and worsening the quality of life. Juglanin, a natural aldose reductase inhibitor, has shown to exhibit anti-inflammatory, anti-nociceptive, and anti-oxidant properties. Objective: The present study was undertaken to evaluate their possible mechanism of action against adjuvant-induced arthritis (AIA), i.e., Freund's complete adjuvant (FCA)-induced arthritis, in experimental rats. Materials and Methods: FCA (0.1 mL) was administered into the subplantar region of female Wistar rats paw to induced AIA. The rats were treated with vehicle (distilled water, 10 mL/kg) or leflunomide (10 mg/kg), or juglanin (10, 20, and 40 mg/kg, respectively) orally for the next 16 days. Various biochemical, molecular, and histological parameters were evaluated to determine the potential of juglanin. Results: Subplantar administration of FCA resulted in a statistically significant (P < 0.05) induction of AIA reflected by alteration in paw volume, joint diameter, paw withdrawal threshold, and paw withdrawal latency, which was statistically significantly inhibited (P < 0.05) by juglanin (20 and 40 mg/kg). It also statistically significantly attenuated (P < 0.05) FCA-induced elevated hepatic oxido-nitrosative stress and mRNA expressions of tumor necrosis factor-alpha (TNF-α), interleukin (IL) IL-1β, IL-6, transforming growth factor-beta (TGF-β), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOs). Western blot analysis revealed that juglanin statistically significantly downregulated (P < 0.05) protein expressions of NF-κB, IκBα, a disintegrin-like and metalloproteinase domain with thrombospondin-1 repeats (ADAMTS)-4, and ADAMTS-5 in hepatic tissue. It also statistically significantly attenuated (P < 0.05) histopathological anomalies induced in the tibiotarsal joint. Conclusion: The present communication suggests that juglanin attenuated altered mechano-tactile allodynia and hyperalgesia via inhibition of elevated oxido-nitrosative stress, cytokines (TNF-α and ILs) levels, immune-inflammatory (TGF-β, NF-κB, Ikβα, COX-2, and iNOs) mediators, and ADAMTS, thus exerting its anti-arthritic potential.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded93    
    Comments [Add]    

Recommend this journal