1. 血管紧张素Ⅱ可促进小鼠激素诱导的缺血性股骨头坏死.
- Author
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刘保一, 李敏德, 杨 帆, 李少鹏, 陈豪杰, and 肖 鹏
- Abstract
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]
- Published
- 2019
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