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Effect of chondroitin sulphate in a rabbit model of atherosclerosis aggravated by chronic arthritis
Author(s) -
HerreroBeaumont G,
Marcos M E,
SánchezPernaute O,
Granados R,
Ortega L,
Montell E,
Vergés J,
Egido J,
Largo R
Publication year - 2008
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/bjp.2008.113
Subject(s) - medicine , arthritis , inflammation , monocyte , proinflammatory cytokine , lesion , ovalbumin , osteoarthritis , ccr2 , endocrinology , thoracic aorta , aorta , ccl2 , chemokine , immunology , pathology , antigen , alternative medicine , chemokine receptor
Background and purpose: Among the agents employed to manage osteoarthritis, chondroitin sulphate (CS) is a natural glycosaminoglycan with an anti‐inflammatory effect on joint cells. CS might also influence the inflammatory component of atherosclerosis. Our aim was to examine the effect of CS administration on vascular injury and on markers of systemic inflammation in a rabbit model of atherosclerosis aggravated by systemic inflammation provoked by chronic antigen‐induced arthritis. Experimental approach: Atherosclerosis was induced in rabbits by maintaining them on a hyperlipidaemic diet after producing an endothelial lesion in the femoral arteries. Simultaneously, chronic arthritis was induced in these animals by repeated intraarticular injections of ovalbumin in previously immunized rabbits. A group of these rabbits were treated prophylactically with CS (100 mg kg −1 day −1 ) and when the animals were killed, serum and peripheral blood mononuclear cells (PBMC) were isolated. Furthermore, femoral arteries and thoracic aorta were used for gene expression studies and histological examination. Key results: CS administration reduced the concentration of the proinflammatory molecules C‐reactive protein and IL‐6 in serum. Likewise, CS inhibited the expression of CCL2/monocyte chemoattractant protein (MCP)‐1 and cyclooxygenase (COX)‐2 in PBMC, and reduced the nuclear translocation of nuclear factor‐κB. In the femoral lesion, CS also diminished the expression of CCL2 and COX‐2, as well as the ratio of the intima/media thickness. Moreover, CS decreased the percentage of rabbits with atherosclerosis and chronic arthritis that developed vascular lesions in the aorta. Conclusions and implications: These findings suggest that CS treatment may to some extent impede the progression of atherosclerosis. British Journal of Pharmacology (2008) 154 , 843–851; doi: 10.1038/bjp.2008.113 ; published online 21 April 2008