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
Highlights
Femoral head necrosis (FHN), a frequentlyencountered lesion, is a disease that causes collapse and dysfunction of femur head as a result of death of cells and changes in its structure
Femoral head necrosis caused by corticosteroids is a pathological process in which the active components of the femur head such as bone cells, bone marrow hematopoietic cells and fat cells die due to excess hormones [2]
Femoral head necrosis caused by cortical steroid refers to the pathological process arising from death of the bioactive components of the femur head such as bone tissue, bone marrow hematopoietic cells and fat cells due to the use of high-dose hormones
Summary
Femoral head necrosis (FHN), a frequentlyencountered lesion, is a disease that causes collapse and dysfunction of femur head as a result of death of cells and changes in its structure. The first case of femoral head necrosis caused by glucocorticoids was reported in the 1950s [3]. The aim of this research was to study the expression levels of apoptosis-related factors in glucocorticoidinduced femoral head necrosis in rats. Corticosterone-induced femoral head necrosis was set up in rats which were injected with endotoxin at a dose of 20 μg/kg twice at an interval of 24 h. Pathological changes in the femoral heads of rats in each group were examined under a light microscope, and the percentage of empty lacunae was calculated. Values of p < 0.05 were regarded as statistically significant
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