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机构地区:[1]中南大学湘雅医院内分泌科,长沙410008 [2]中南大学湘雅二医院代谢内分泌研究所,长沙410011
出 处:《中南大学学报(医学版)》2008年第8期731-736,共6页Journal of Central South University :Medical Science
摘 要:目的:研究脂联素对成骨细胞的分化作用。方法:免疫印迹检测体外培养成骨细胞脂联素受体(adiponectin receptor,AdipoR)表达。用酶联免疫吸附试验检测碱性磷酸酶(alkaline phosphatase,ALP)活性;用放射免疫测定法测定骨钙素(osteocalcin,OC);并观测脂联素对矿化的影响。用siRNAs抑制AdipoR1表达,观察脂联素对成骨细胞分化作用的变化。结果:检测到成骨细胞AdipoR1蛋白表达。脂联素可提高ALP活性和促进OC分泌,并促进矿化结节形成,此作用可被AdipoR1的siRNAs转染抑制。脂联素作用于成骨细胞可诱导p38和JNK磷酸化,而p38抑制剂SB203580可减轻其对成骨细胞ALP活性的影响。结论:脂联素通过诱导p38信号转导途径诱导人成骨细胞分化。Objective To investigate the effect of adiponectin on the osteoblast differentiation and its signal transduction. Methods Adipopnectin receptor (AdipoR) was detected by immunoblot analysis. Alkaline phosphatase (ALP) activity was measured by enzyme-linked immunosorbent as- say. Osteocalcin was measured by a specific radioimmunoassay kit, and the extent of mineralized matrix was determined. RNA interference was used to down-regulate the expression of AdipoR1 in human osteoblasts, and the effect of adiponectin on osteoblast differentiation was investigated. Results Only AdipoR1 protein was detected in human osteoblasts. Adiponectin could promote osteoblast differentiation, and result in a dose-dependent increase in ALP activity, osteocalcin secretion, and an increase in mineralized nodules. Suppression of AdipoR1 with siRNA could abolish the adiponectin induced ALP expression. Adiponectin could induce the activation of p38 and JNK, but not ERK1/2 in osteoblasts, and the pretreatment of osteoblasts with the p38 inhibitor (SB203580) could block the adiponectin-induced ALP activity. Conclusion Adiponectin can induce human osteoblast differentiation via AdipoR 1/p38 pathway.
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