摘要
目的观察葡萄糖对大鼠骨髓破骨细胞骨吸收功能的影响,探讨糖尿病骨质疏松的发病机制。方法用巨噬细胞集落刺激因子、RANKL诱导大鼠骨髓单个核细胞分化为破骨细胞,同时给予不同浓度的葡萄糖(0、5.5、15、25mmol/L)干预,通过观察骨吸收陷窝数量和面积比及破骨细胞膜表面整合素ανβ3(CD61)表达水平分析葡萄糖对破骨细胞骨吸收功能的影响,结果(1)高糖(25mmol/L)组培养7d骨吸收陷窝数量和面积比与其他3组相比明显增多(P〈0.05或P〈0.01)。(2)高糖组破骨细胞膜表面CD61表达量及平均荧光强度3d时与其他3组相比均明显上调(P〈0.05或P〈0.01);5、7d时与对照组(0mmol/L)相比明显上调(P〈0.05)。结论高糖可增强破骨细胞的骨吸收功能,这可能是糖尿病骨质疏松的发病机制之一。
Objective To observe the effect of glucose on bone resorption by osteoclasts derived from rat bone marrow cells, and to study the role of glucose in the pathogenesis of diabetic osteoporosis. Methods Mononuclear cells from rat bone marrow were incubated with α-MEM containing macrophage colony stimulating factor(M-CSF) and receptor activator of NF-κB ligand( RANKL). The culture was treated with glucose of different concentrations(0,5.5,15,25 mmol/L). The effect of glucose on bone resorption by osteoclast was studied by analyzing absorptive lacuna and the expression of integrin ανβ3 ( CD61 ). Results ( 1 ) The amount and area ratio of bone absorptive lacuna in high glucose(25 mmol/L)group showed significant difference from the other 3 groups at day 7 (P〈0.05 or P〈0.01 ). (2)The expression of CD61 in osteoclast were up-regulated in high glucose group compared with the other 3 groups at day3 (P〈0.05 or P〈0.01 ),and showed signifcant difference with the control (0 mmol/L)group at day 5and 7 (P〈 0. 05 ). Conclusion High glucose may enhance bone resorption by osteoclasts,suggesting that this may be one of the key pathogenetic factors of diabetic osteoporosis.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2009年第5期549-551,共3页
Chinese Journal of Endocrinology and Metabolism