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BACKGROUND: Asparaginase can inhibit angiogenesis and affect blood supply, and make damage to the vascular endothelial cells, thereby affecting the local blood supply of femoral head. OBJECTIVE: To investigate the effect of asparaginase on the avascular necrosis of femoral head induced by dexamethasone. METHODS: Balb/c male mice were provided by Laboratory Animal Center of Dalian Medical University, and the study was approved by the Experimental Ethics Committee of Affiliated Zhongshan Hospital of Dalian University. Sixty male Balb/c mice were randomly divided into four groups: asparaginase + dexamethasone group (n=15, 2 mg/L dexamethasone in the water, and intraperitoneal injection of 1 200 U/kg asparaginase), asparaginase group (n=15, intraperitoneal injection of 1 200 U/kg asparaginase), dexamethasone group (n=15, 2 mg/L dexamethasone in the water), and control group (n=15, no intervention). All mice were killed after 8 weeks. The body mass, coagulation factors, hematoxylin-eosin staining and immunohistochemical staining of the femoral head were observed. RESULTS AND CONCLUSION: (1) The body mass gain in the asparaginase + dexamethasone group was significantly lower than that in the other three groups. (2) The levels of coagulation factor III and V in the asparaginase + dexamethasone group were significantly higher than those in the other three groups (P < 0.05 or P < 0.01). (3) Compared with the other three groups, the empty bone lacunae rate was increased (P < 0.05), and trabecular fracture rate was decreased (P < 0.05), and the degree of osteonecrosis was more obvious in the asparaginase + dexamethasone group. (4) The absorbance value of osteoprotegerin in the asparaginase + dexamethasone group was significantly lower than that in the other three groups (P < 0.05 or P < 0.01). (5) These results indicate that asparaginase can promote avascular necrosis of femoral head in mice. [ABSTRACT FROM AUTHOR]

BACKGROUND: There are many studies on the pathogenesis of steroid-induced avascular necrosis of the femoral head, but the relevant mechanisms remain unclear. Local obstruction of blood flow to the femoral head is an important cause of avascular necrosis of the femoral head. OBJECTIVE: To investigate the effect of angiotensin II on avascular necrosis of the femoral head. METHODS: Male Balb/c mice were randomly divided into three groups. In the dexamethasone plus angiotensin II group, 2 mg/L dexamethasone was added in drinking water, subcutaneous implantatian with osmotic pump capsules began on the first day, followed by pumping with 0.28 mg/(kg?d) angiotensin II for 4 weeks. Dexamethasone group dosage and usage were the same as dexamethasone plus angiotensin II group. Control group had normal feed. All mice were fed for 6 weeks. RESULTS AND CONCLUSION: (1) General condition and pathological changes showed that compared with the dexamethasone and control groups, the body mass increase was significantly decreased, and the serum total cholesterol, total triglyceride, empty lacunae rate and bone volume/tissue volume were significantly increased in the dexamethasone plus angiotensin II group (P < 0.05), and the degree of osteonecrosis was more obvious. (2) Immunohistochemical results showed that the osteoprotegerin protein expression level in the dexamethasone plus angiotensin II group was significantly higher than that in the other two groups (P < 0.05), indicating that the osteoclast was more active. (3) In summary, angiotensin II can obviously promote steroid-induced avascular necrosis of the femoral head in mice. [ABSTRACT FROM AUTHOR]