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Ellagic acid alleviates adjuvant induced arthritis by modulation of pro- and anti-inflammatory cytokines

View Article: PubMed Central - PubMed

ABSTRACT

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology, but it is now clear that pro-inflammatory cytokines play a central role in its pathogenesis. Ellagic acid (EA) has a variety of biological activities including anti-oxidant, anti-inflammatory, and anti-cancer properties. The aim of the present study was to evaluate the potential effect of ellagic acid on the prevention and/or treatment of adjuvant induced arthritis (AIA) model in mice. Ellagic acid treatment was started one week before AIA induction and continued for three weeks after induction of AIA. Ellagic acid treatment significantly (p < 0.01) inhibited foot paw oedematous swelling and attenuated AIA-associated pathology. Ellagic acid significantly (p < 0.01) reduced serum levels of pro-inflammatory cytokines: interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), and interleukin 17 (IL-17). However, serum levels of IL-10 and interferon γ (IFN-γ) significantly increased (p < 0.01 and p < 0.05, respectively), while serum level of transforming growth factor β (TGF-β) did not significantly alter with EA treatment. In conclusion, these results suggest that EA attenuated AIA-associated pathology in the mouse model by downregulation of pro-inflammatory cytokines and upregulation of anti-inflammatory cytokines.

No MeSH data available.


Related in: MedlinePlus

Representative photomicrographs showing the histopathological picture of hind paws and digits of arthritic control (AC) and arthritic treated (AT) mice in H&E stained sections (× 400). AC mice showed hyperplastic synovial membrane composed of multiple layers of synoviocytes (AC-a), marked pannus formation and fibroplasia of the underlying connective tissues associated with cartilage erosion and bone resoprption (AC-b), and multiple panni were formed from synovial membrane (AC-c). However, AT mice revealed mild pannus formation, fibroplasias, cartilage erosion and bone resoprption (AT)
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f0002: Representative photomicrographs showing the histopathological picture of hind paws and digits of arthritic control (AC) and arthritic treated (AT) mice in H&E stained sections (× 400). AC mice showed hyperplastic synovial membrane composed of multiple layers of synoviocytes (AC-a), marked pannus formation and fibroplasia of the underlying connective tissues associated with cartilage erosion and bone resoprption (AC-b), and multiple panni were formed from synovial membrane (AC-c). However, AT mice revealed mild pannus formation, fibroplasias, cartilage erosion and bone resoprption (AT)

Mentions: Concerning AC mice, microscopic examination showed synovitis characterised by proliferating synovial lining cells, in 2-3 layers, as well as proliferation of the underlying blood vessels, which was associated with perivascular oedema and diffuse cellular infiltrates composed of mononuclear cells (Fig. 2A). In many specimens, the inflammatory cellular exudates extended to involve whole periarticular soft tissues of the connective tissue and muscles. There was synovial sloughing in some areas of synovial membrane and mild proliferative lesion of fibroblast-like cells. Pannus formation was in the form of single or multiple proliferating granulation tissues containing hyperplastic synoviocytes and inflammatory cells at the articular cartilage margin, and at the cartilage-bone level. The articular cartilages of some arthritic mice had uneven articular surface and demonstrated superficial fibrillation accompanied by cell death or proliferation and in some cases extended to the mid-zone portion of the articular cartilage. Moreover, the articular bone destruction was visualised by osteoclast activity and fibroplasia (Fig. 2). However, AT mice showed the previously mentioned histopathological lesions of arthritis, but with mild to moderate degree (Fig. 2, AT).


Ellagic acid alleviates adjuvant induced arthritis by modulation of pro- and anti-inflammatory cytokines
Representative photomicrographs showing the histopathological picture of hind paws and digits of arthritic control (AC) and arthritic treated (AT) mice in H&E stained sections (× 400). AC mice showed hyperplastic synovial membrane composed of multiple layers of synoviocytes (AC-a), marked pannus formation and fibroplasia of the underlying connective tissues associated with cartilage erosion and bone resoprption (AC-b), and multiple panni were formed from synovial membrane (AC-c). However, AT mice revealed mild pannus formation, fibroplasias, cartilage erosion and bone resoprption (AT)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5382880&req=5

f0002: Representative photomicrographs showing the histopathological picture of hind paws and digits of arthritic control (AC) and arthritic treated (AT) mice in H&E stained sections (× 400). AC mice showed hyperplastic synovial membrane composed of multiple layers of synoviocytes (AC-a), marked pannus formation and fibroplasia of the underlying connective tissues associated with cartilage erosion and bone resoprption (AC-b), and multiple panni were formed from synovial membrane (AC-c). However, AT mice revealed mild pannus formation, fibroplasias, cartilage erosion and bone resoprption (AT)
Mentions: Concerning AC mice, microscopic examination showed synovitis characterised by proliferating synovial lining cells, in 2-3 layers, as well as proliferation of the underlying blood vessels, which was associated with perivascular oedema and diffuse cellular infiltrates composed of mononuclear cells (Fig. 2A). In many specimens, the inflammatory cellular exudates extended to involve whole periarticular soft tissues of the connective tissue and muscles. There was synovial sloughing in some areas of synovial membrane and mild proliferative lesion of fibroblast-like cells. Pannus formation was in the form of single or multiple proliferating granulation tissues containing hyperplastic synoviocytes and inflammatory cells at the articular cartilage margin, and at the cartilage-bone level. The articular cartilages of some arthritic mice had uneven articular surface and demonstrated superficial fibrillation accompanied by cell death or proliferation and in some cases extended to the mid-zone portion of the articular cartilage. Moreover, the articular bone destruction was visualised by osteoclast activity and fibroplasia (Fig. 2). However, AT mice showed the previously mentioned histopathological lesions of arthritis, but with mild to moderate degree (Fig. 2, AT).

View Article: PubMed Central - PubMed

ABSTRACT

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology, but it is now clear that pro-inflammatory cytokines play a central role in its pathogenesis. Ellagic acid (EA) has a variety of biological activities including anti-oxidant, anti-inflammatory, and anti-cancer properties. The aim of the present study was to evaluate the potential effect of ellagic acid on the prevention and/or treatment of adjuvant induced arthritis (AIA) model in mice. Ellagic acid treatment was started one week before AIA induction and continued for three weeks after induction of AIA. Ellagic acid treatment significantly (p < 0.01) inhibited foot paw oedematous swelling and attenuated AIA-associated pathology. Ellagic acid significantly (p < 0.01) reduced serum levels of pro-inflammatory cytokines: interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), and interleukin 17 (IL-17). However, serum levels of IL-10 and interferon γ (IFN-γ) significantly increased (p < 0.01 and p < 0.05, respectively), while serum level of transforming growth factor β (TGF-β) did not significantly alter with EA treatment. In conclusion, these results suggest that EA attenuated AIA-associated pathology in the mouse model by downregulation of pro-inflammatory cytokines and upregulation of anti-inflammatory cytokines.

No MeSH data available.


Related in: MedlinePlus