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Exercise modulates the expression of IL-1β and IL-10 in the articular cartilage of normal and osteoarthritis-induced rats

Authors :
Carlos Lavalle-Montalvo
José Manuel Hernández-Hernández
Mariel Rojas-Ortega
Raymundo Cruz
Moisés Cabrera-González
Juan B. Kouri
M. A. Vega-Lopez
Source :
Pathology - Research and Practice. 211:435-443
Publication Year :
2015
Publisher :
Elsevier BV, 2015.

Abstract

After a joint lesion, high-impact exercise is a risk factor for the development of osteoarthritis (OA). The degradation of articular cartilage in OA has been associated with the activation of inflammatory cytokine signaling pathways. However, differences in cytokine expression in healthy and injured cartilage after exercise have not yet been analyzed. We used immunofluorescence and Western blot to study the expression of IL-1β and IL-10 in the articular cartilage of normal (N), sham-operated (S), and menisectomized (OA) rats subjected or not to high-impact exercise (E) for 3, 6, and 10 days (N, NE, S, SE, and OA groups). Cartilage integrity and proteoglycan content were only affected in the OA groups. Exercise increased the amount of IL-1β and IL-10 positive chondrocytes in NE and SE groups compared with non-exercised groups (N and S). The expression of IL-1β was up-regulated over time in the NE and OA groups, although in the late stages the increase was higher in the OA groups. In contrast, the expression of anti-inflammatory IL-10 was low in the OA group, whereas in the NE groups expression levels were higher at each time point analyzed. These results suggest that anti- and pro-inflammatory molecules in the cartilage might be tightly regulated to maintain the integrity of the tissue and that when this equilibrium is broken (when the meniscus is removed), the pro-inflammatory cytokines take over and OA develops.

Details

ISSN :
03440338
Volume :
211
Database :
OpenAIRE
Journal :
Pathology - Research and Practice
Accession number :
edsair.doi.dedup.....cc869b432c2e0f654c8320c11bbc660f
Full Text :
https://doi.org/10.1016/j.prp.2015.01.008