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75 Moringa oleifera lam ameliorates adjuvant induced arthritis via inhibition of inflammatory mediators and down-regulation of mmp3 and mmp-9 proteins
  1. P Pandey1,
  2. PC Bhatt2 and
  3. V Kumar1
  1. 1Sam Higginbottom Institute of Agriculture – Technology and Sciences, Department of Pharmaceutical Sciences, Allahabad, India
  2. 2JAMIA HAMDARD, pharmacognosy and phytochemistry, Delhi, India

Abstract

Background and aims Rheumatoid arthritis (RA) is an autoimmune disease, which induces systematic and typical inflammation and affects 1% younger population Worldwide. Natural products are being preferred over the available treatment regimes for arthritis. Moringa oleifera has been very popular ethanomedicine for the treatment of inflammatory disorders in North-eastern part of India. With this background, the current investigation was carried out to scrutinise the anti-arthritic potential of Moringa oleifera in complete fruend’s adjuvant (CFA) induced arthritis animal model.

Methods In the present investigation, we used the CFA, turpentine and formaldehyde into the sub-plantar region of hind paw of rats for induction of arthritis. After induction, joint diameter, arthritis score and body weight were estimated at regular interval. We studied the effect of plant extract on pro-inflammatory cytokines and inflammatory mediator, respectively. Histological architecture and other changes were also studied.

Results Oral treatment of MO at doses of 25, 50 and 100 mg/kg significantly (p<0.001) down-regulated joint inflammation as evidenced via reduction in the joint diameter, arthritic score and inflammatory cell infiltration.

Conclusions MO treatment were found to reduce pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and inflammatory mediators PGE2 and COX-2 in a dose dependent manner. MO also down-regulated the NF-kB in adjuvant immunised joint. Apart from these findings MO abrogated degrading enzymes, which was evident from down-regulated protein expression of MMP-3 and MMP-9. Our findings clearly indicate the anti-arthritic potential of MO via inhibition of NF-kB pathway.

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