title: The effects of physical activity on apoptosis and lubricin expression in articular cartilage in rats with glucocorticoid-induced osteoporosis.
abstract: Glucocorticoids are considered the most powerful anti-inflammatory and immunomodulating drugs. However, a number of side-effects are well documented in different diseases, including articular cartilage, where increases or decreases in the synthesis of hormone-dependent extracellular matrix components are seen. The objective of this study has been to test the effects of procedures or drugs affecting bone metabolism on articular cartilage in rats with prednisolone-induced osteoporosis and to evaluate the outcomes of physical activity with treadmill and vibration platform training on articular cartilage. The animals were divided into 5 groups, and bone and cartilage evaluations were performed using whole-body scans and histomorphometric analysis. Lubricin and caspase-3 expression were evaluated by immunohistochemistry, Western blot analysis and biochemical analysis. These results confirm the beneficial effect of physical activity on the articular cartilage. The effects of drug therapy with glucocorticoids decrease the expression of lubricin and increase the expression of caspase-3 in the rats, while after physical activity the values return to normal compared to the control group. Our findings suggest that it might be possible that mechanical stimulation in the articular cartilage could induce the expression of lubricin, which is capable of inhibiting caspase-3 activity, preventing chondrocyte death. We can assume that the physiologic balance between lubricin and caspase-3 could maintain the integrity of cartilage. Therefore, in certain diseases such as osteoporosis, mechanical stimulation could be a possible therapeutic treatment. With our results we can propose the hypothesis that physical activity could also be used as a therapeutic treatment for cartilage disease such as osteoarthritis.
authors.affiliation: Department of Bio-Medical Sciences, Human Anatomy and Histology Section, University of Catania, Catania, Italy. g.musumeci@unict.it
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Musumeci
authors.forename: Carla
authors.initials: C
authors.lastname: Loreto
authors.forename: Rosalia
authors.initials: R
authors.lastname: Leonardi
authors.forename: Sergio
authors.initials: S
authors.lastname: Castorina
authors.forename: Salvatore
authors.initials: S
authors.lastname: Giunta
authors.forename: Maria Luisa
authors.initials: ML
authors.lastname: Carnazza
authors.forename: Francesca Maria
authors.initials: FM
authors.lastname: Trovato
authors.forename: Karin
authors.initials: K
authors.lastname: Pichler
authors.forename: Annelie Martina
authors.initials: AM
authors.lastname: Weinberg
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D001823:Body Composition; D002358:Cartilage, Articular / Q000201:enzymology / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D005938:Glucocorticoids / Q000009:adverse effects*; D006023:Glycoproteins / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism* / Q000473:pathology; D010805:Physical Conditioning, Animal; D011239:Prednisolone / Q000009:adverse effects; D051381:Rats; D017208:Rats, Wistar; D000099158:Proteoglycan 4
chemical_list: D053148:Caspase 3; D005938:Glucocorticoids; D006023:Glycoproteins; D011239:Prednisolone; D000099158:Proteoglycan 4