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作 者:李月白[1] 殷力[2] 王义生[2] 李杰[2] 秦国斌[3] 孟宪中[2] 许建中[2]
机构地区:[1]河南医科大学基础医学院生化教研室,郑州450052 [2]河南医科大学第一附属医院骨科 [3]安阳市第一人民医院骨科
出 处:《中华骨科杂志》1999年第11期687-689,共3页Chinese Journal of Orthopaedics
基 金:河南省科委自然科学基金!984024900
摘 要:观察激素诱导骨髓基质细胞分化成脂肪细胞的作用,揭示激素性股骨头缺血性坏死的病理学机制。方法 采用原代骨髓基质细胞体外培养技术,取小鼠双侧股骨骨髓细胞,通过细胞贴壁、分离获取骨髓基质细胞。以地塞米松作为脂肪细胞分化诱导剂处理细胞,苏丹Ⅲ染色,光镜下脂肪细胞计数。结果以递增浓度(0、1× 10~-9、1× 10~-8、1× 10~-7、1× 10~-6 mol/L)地塞米松处理细胞并培养 21天后, 1×10~-6 mol/L组中诱导分化生成的脂肪细胞最多,对照组中脂肪细胞最少,各组脂肪细胞随地塞米松浓度增大而增多,具有一定的剂量依赖性。实验组细胞经高浓度(1×10~-7 mol/L)地塞米松处理并培养12天后,其细胞内碱性磷酸酶活性明显低于对照组,两者差异有非常显著性意义(P<0.01)。结论 地塞米松能够直接诱导骨髓基质细胞大量分化成脂肪细胞,其成骨分化减少,这可能是大剂量应用激素后股骨头骨髓内脂肪组织增多,骨内压升高,导致骨微循环障碍,同时骨修复过程缓慢,从而发生股骨头缺血性坏死的原因。Objective To observe steroid-induced marrow stromal cell differentiation into adipocytes to elucidate the pathogenesis of the steroid-induced avascular necrosis of the femoral head. Methods The primary marrow stromal cells of the femur of the mouse were procured and cultured. The samples were isolated; after adherent growth culture in vitro, and were treated with dexamethasone which acted as adipocyte differ- entiation inducer. The cells in culture were stained with Sudan Ⅲ. The number of adipocytes were counted on a light microscope. Results After the cells in culture were treated with increasing(0, 1 × 10^-9, 1 × 10^-8, 1 × 10^-7, and 1 × 10^-6 mol/L) concentrations of dexamethasone for 21 days, the number of adipocytes, which was highest in 1 ×10^- 6 mol/L groups and lowest in the control, increased with higher concentrations of dexamethasone and showed a dose-dependent relation. Alkaline phosphatase activity in the cells exposed to higher concentration of dexamethasone(1 × 10^-7 mol/L) for 12 days was significantly lower than that in the control (P < 0. 01 ). Conclusion Dexamethasone can directly induce marrow stromal cell differentiation into a large number of adipocytes and inhibit osteogenic differentiation. This might lead to an increase in marrow fat volume of the femoral head following administration of high dose of steroids; eventually an increase of intraosseous pressure occurred, with a decrease of vascular perfusion. Without sufficient repair of the necrotic bone, the final result is avascular necrosis of the femoral head.
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