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Published:
Mar 17, 2021DOI:
10.4314/tjpr.v20i1.8Keywords:
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Main Article Content
Expression levels of apoptotic factors in a rat model of corticosteroid-induced femoral head necrosis
Abstract
Purpose: To study the expression levels of apoptotic factors in corticosteroid-mediated femoral head necrosis (FHN) in rats.
Methods: Sprague-Dawley (SD) rats (n = 60) bred adaptively for one week were randomly assigned to control and model groups (30 rats/group). A rat model of corticosteroid-induced femoral head necrosis was established. Then, 3 mL of blood drawn from the inferior vena cava of each rat was used for the assay of the expression levels of osteoprotegerin (OPG) and osteoclast differentiation factor (RANKL) in each group using enzyme-linked immunosorbent assay (ELISA). The caspase-3- and Bcl-2-+ve cells in each group were determined with immunohistochemical method.
Results: Relative to control, serum OPG level of model group was significantly decreased, while the RANKL level was markedly raised (p < 0.05). The degree of empty lacunae in the model rats was markedly increased, relative to control. Caspase-3-+ve cells were more numerous in the model group than in control, while Bcl-2-positive cells were markedly decreased compared to control (p < 0.05).
Conclusion: Apoptosis occurs in the rat model of femoral head necrosis. Glucocorticoids may regulate the apoptotic process by upregulating caspase-3 and inhibiting Bcl-2. This provides a novel lead for FHN therapy.
Keywords: Femoral head necrosis, Corticosteroid, Glucocorticoid, Apoptosis
