Abstract
Purpose: To investigate the effectiveness of luteolin treatment in postmenopausal model of osteoarthritis (OA)Methods: Sprague-Dawley rats were divided into five groups. Luteolin was given orally to rats at doses of 50 and 100 mg/kg for 4 months, while aceclofenac was administered at a dose of 10 mg/kg. The antiinflammatory and anti-arthritic effects of luteolin and aceclofenac were determined using paw-withdrawal method. Knee joint thickness was measured using X-ray imaging. Pathological changes in bone slices were determined with immuno-histochemical evaluation. The levels of inflammatory cytokines were assessed by reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis.Results: Oral ingestion of luteolin significantly reduced manifestations of OA and suppressed levels of serum cytokines (p < 0.05). Moreover, luteolin increased expression of bone marker protein and reduced the gene expression levels of matrix metalloproteinases (MMPs, p < 0.05), suggesting its protective effects on chondrocytes. Luteolin significantly reduced the production of inflammatory chemokines and cytokines (IFN-γ, IL-1, and IL-6). Histopathological examination showed that luteolindecreased pathological lesions in monoiodoacetate-mediated OA in ovariectomized rats, indicatingprevention of cartilage loss.Conclusion: These results suggest that luteolin exerts protective effects against monoiodoacetateinduced (MIA) OA in ovariectomized rats by suppressing the expressions of inflammation-related mediators (IL-1β, Cox-2, and PGE-2). Thus, luteolin is a prospective option for the suppression of postmenopausal OA in humans.
Highlights
Osteoarthritis (OA) is one of the most common degenerative disorders
No marked decreases in body weight were noticed in rats treated with luteolin (50 and 100 mg/kg) and aceclofenac at the end of the 4-week study, when compared to MIA-induced OA and ovariectomized rats treated with vehicle (Figure 1 A)
The anti-inflammatory and anti-catabolic effects of luteolin on chondrocyte mRNA expressions were investigated with reverse transcription-polymerase chain reaction (RT-PCR)
Summary
Osteoarthritis (OA) is one of the most common degenerative disorders. It manifests in clinical changes such as cartilage loss and inflammation of synovial fluid. Chondrocytes respond to OAinduced inflammation by increasing sub-chondral matrix biosynthesis and releasing antiinflammatory mediators, resulting in OA progression. Chondrocytes and synovial cells together produce proinflammatory cytokines which influence apoptosis of chondrocytes [1]. Several animal models have been used to investigate the pathogenesis of OA, as well as treatment approaches. Ovariectomy is one of the most used strategies for induction of OA [2]. When ovariectomized rats are injected with monoiodoacetate (MIA), they turn into spontaneously advanced OA model
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