目的研究初发系统性红斑狼疮(systemic lupus erythematosus,SLE)患者外周血淋巴细胞中细胞核因子-κB受体激活剂配体(receptor activator of nuclear factor kappa B ligand,RANKL)、护骨素(osteoprotegerin,OPG)基因mRNA的...目的研究初发系统性红斑狼疮(systemic lupus erythematosus,SLE)患者外周血淋巴细胞中细胞核因子-κB受体激活剂配体(receptor activator of nuclear factor kappa B ligand,RANKL)、护骨素(osteoprotegerin,OPG)基因mRNA的表达情况,探讨其表达水平与初发SLE患者骨质疏松的关系。方法选择初发SLE患者45例及正常对照42例,运用实时定量PCR方法检测患者外周血淋巴细胞RANKL、OPG的mRNA表达水平。采用双能X线骨密度仪分别检测患者腰椎(L1-4)和股骨近端2个部位的骨密度,单因素分析RANKL、OPG基因mRNA表达水平与SLE患者骨密度的关系。结果SLE患者RANKL、OPG基因mRNA表达水平较正常对照组明显减低(P〈0.01);SLE患者2个部位的骨密度均低于正常对照组(P〈0.05),骨量异常发生率为28-89%,骨量异常降低的SLE患者OPG基因mRNA的表达水平比骨量正常的患者显著降低,两者间的差异有统计学意义(P〈0.01);而RANKL基因mRNA表达水平的差异无统计学意义(P〉0.05);OPG基因mRNA表达水平与初发SLE患者骨密度间存在正相关(r=0.461;P=0.001),即OPG表达水平越低,骨量减少越明显;而RANKL基因mRNA表达降低与初发SLE患者骨密度无明显相关性(r=-0.189,P=0.214);初发SLE患者疾病活动度与骨量减少、RANKL及OPG基因表达水平间不存在相关性(r=0.293,P=0.138;r=-0.099,P=0.493;,=0.138,P=0.493)。结论初发SLE患者骨量减少的发病率较正常人群增高,并且初发SLE患者体内RANKL和OPG基因表达存在异常;其中OPG表达水平的降低可能与初发SLE患者的骨量减少有密切关系。展开更多
目的分析血清骨保护素(osteoprotegerin,OPG)、核因子κB活化因子配体(receptor-activator of nuclear factor kappa B ligand,RANKL)及雌二醇(estradiol,E_2)对运动性骨疲劳的早期筛查价值。方法健康雌性大鼠随机分为对照组和实验组,8...目的分析血清骨保护素(osteoprotegerin,OPG)、核因子κB活化因子配体(receptor-activator of nuclear factor kappa B ligand,RANKL)及雌二醇(estradiol,E_2)对运动性骨疲劳的早期筛查价值。方法健康雌性大鼠随机分为对照组和实验组,8周训练结束后处死大鼠,采用酶联免疫法检测血清RANKL、OPG和E_2水平,采用IBM 21.0 SPSS绘制受试者工作特征曲线曲线(receiver operating characteristic curve,ROC曲线),计算它们的ROC曲线下面积(area under the curve,AUC)、灵敏度和特异度,根据约登指数确定其诊断界值并评价筛查价值。结果血清RANKL、OPG、OPG/RANKL比值及E_2的AUC均大于0.9。选定的血清RANKL、OPG、OPG/RANKL比值和E_2的诊断界值分别为96.245 ng/ml、2.383 ng/ml、0.028和105.293 pg/ml,其灵敏度和特异度分别为90.21%和45.22%、96.19%和51.07%、94.42%和56.69%、93.36%和40.71%。血清RANKL、OPG、OPG/RANKL比值和E_2均早于金标准出现阳性诊断结果。结论动态检测血清RANKL、OPG及E_2水平,有望实现运动性骨疲劳的早期预警。展开更多
目的:研究人牙囊细胞白细胞介素-10(interleukin-10,IL-10)蛋白的表达及其对破骨细胞分化因子(receptor activator of nuclear factor kappa B ligand,RANKL)表达的影响。方法:采用组织块加胶原酶消化法培养人牙囊细胞,进行IL-10免疫组...目的:研究人牙囊细胞白细胞介素-10(interleukin-10,IL-10)蛋白的表达及其对破骨细胞分化因子(receptor activator of nuclear factor kappa B ligand,RANKL)表达的影响。方法:采用组织块加胶原酶消化法培养人牙囊细胞,进行IL-10免疫组化染色。25ng/mlIL-10作用于牙囊细胞0、1、3、6 h,用RT-PCR检测RANKL mRNA表达的变化。结果:人牙囊细胞IL-10表达阳性。25ng/ml IL-10降低人牙囊细胞RANKL的表达,且具有时间依赖性。结论:人牙囊细胞表达IL-10,IL-10通过降低人牙囊细胞RANKL的表达,在牙齿萌出过程中起重要的调控作用。展开更多
Objective: To investigate the effects of anastrozole combined with Shuganjiangu decoction on osteoblast-like cells. Methods: Human osteoblast-like cells MG-63 were cultured and divided into four groups control, an...Objective: To investigate the effects of anastrozole combined with Shuganjiangu decoction on osteoblast-like cells. Methods: Human osteoblast-like cells MG-63 were cultured and divided into four groups control, anastrozole, Shuganjiangu decoction (SGJGD), and anastrozole combined with SGJGD. Cell proliferation was investigated by M-IF assay. Alkaline phosphatase (ALP) and osteocalcin, the indicators of cell differentiation, were evaluated by p-nitrophenyl- phosphate method and radioimmunoassay, respectively. Gene expressions of ALP, osteocalcin, osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) were examined by real-time PCR. Results: As evidenced by MTT assay, cell proliferation of MG-63 was inhibited by anastrozole, but stimulated with treatment of SGJGD alone and combined with anastrozole (P〈O.01). Compared with control group, ALP activity was increased by the treatment of SGJGD alone and combined with anastrozole (P〈0.01). Also, osteocalcin secretion was enhanced with the treatment of SGJGD single and combination with anastrozole (P〈O.05). In the real-time PCR assay, gene expressions of ALP and osteocalcin were significantly increased (P〈0.01 for ALP, P〈0.05 for osteocalcin) by the treatment of SGJGD and anastrozole combined with SGJGD, but the expression of RANKL was decreased (P〈O.05). Moreover, anastrozole combined with SGJGD upregulated gene expression of OPG (P〈O.01). Conclusion: SGJGD may alleviate the injury effects of anastrozole on MG-63 cells through adjusting bone formation and resorption indicators.展开更多
骨骼是一个动态组织,在生物的整个生命周期中不断地进行构建、吸收、重建,核因子(nucler factor,NF)κB受体活化因子(receptor activator of NF-κB,RANK)/NF-κB受体活化因子配体(receptor activator of NF-κB ligand,RANK...骨骼是一个动态组织,在生物的整个生命周期中不断地进行构建、吸收、重建,核因子(nucler factor,NF)κB受体活化因子(receptor activator of NF-κB,RANK)/NF-κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)/护骨素(osteoprotegerin,OPG)系统是调控这一过程的关键系统。RANK/RANKL/OPG属于肿瘤坏死因子及其受体超家族,三者通过调控破骨细胞的分化和活化来影响骨吸收和重建的过程。另外,免疫细胞也参与和调节RANK/RANKL的表达和分泌,而免疫细胞本身亦受到该系统的影响,因此,RANK/RANKL/OPG系统成为骨和免疫之间的重要关联。RANK/RANKL/OPG系统的失衡与多种骨代谢性疾病及免疫系统疾病引发的继发性骨病密切相关,该系统的发现为研究相关疾病的病理机制和治疗方法提供了基础。由此建立的抗RANKL疗法已经开始应用于临床试验和研究。此文对RANK/RANKL/OPG系统、系统相关疾病以及抗RANKL治疗的进展做一综述。展开更多
文摘目的研究初发系统性红斑狼疮(systemic lupus erythematosus,SLE)患者外周血淋巴细胞中细胞核因子-κB受体激活剂配体(receptor activator of nuclear factor kappa B ligand,RANKL)、护骨素(osteoprotegerin,OPG)基因mRNA的表达情况,探讨其表达水平与初发SLE患者骨质疏松的关系。方法选择初发SLE患者45例及正常对照42例,运用实时定量PCR方法检测患者外周血淋巴细胞RANKL、OPG的mRNA表达水平。采用双能X线骨密度仪分别检测患者腰椎(L1-4)和股骨近端2个部位的骨密度,单因素分析RANKL、OPG基因mRNA表达水平与SLE患者骨密度的关系。结果SLE患者RANKL、OPG基因mRNA表达水平较正常对照组明显减低(P〈0.01);SLE患者2个部位的骨密度均低于正常对照组(P〈0.05),骨量异常发生率为28-89%,骨量异常降低的SLE患者OPG基因mRNA的表达水平比骨量正常的患者显著降低,两者间的差异有统计学意义(P〈0.01);而RANKL基因mRNA表达水平的差异无统计学意义(P〉0.05);OPG基因mRNA表达水平与初发SLE患者骨密度间存在正相关(r=0.461;P=0.001),即OPG表达水平越低,骨量减少越明显;而RANKL基因mRNA表达降低与初发SLE患者骨密度无明显相关性(r=-0.189,P=0.214);初发SLE患者疾病活动度与骨量减少、RANKL及OPG基因表达水平间不存在相关性(r=0.293,P=0.138;r=-0.099,P=0.493;,=0.138,P=0.493)。结论初发SLE患者骨量减少的发病率较正常人群增高,并且初发SLE患者体内RANKL和OPG基因表达存在异常;其中OPG表达水平的降低可能与初发SLE患者的骨量减少有密切关系。
文摘目的分析血清骨保护素(osteoprotegerin,OPG)、核因子κB活化因子配体(receptor-activator of nuclear factor kappa B ligand,RANKL)及雌二醇(estradiol,E_2)对运动性骨疲劳的早期筛查价值。方法健康雌性大鼠随机分为对照组和实验组,8周训练结束后处死大鼠,采用酶联免疫法检测血清RANKL、OPG和E_2水平,采用IBM 21.0 SPSS绘制受试者工作特征曲线曲线(receiver operating characteristic curve,ROC曲线),计算它们的ROC曲线下面积(area under the curve,AUC)、灵敏度和特异度,根据约登指数确定其诊断界值并评价筛查价值。结果血清RANKL、OPG、OPG/RANKL比值及E_2的AUC均大于0.9。选定的血清RANKL、OPG、OPG/RANKL比值和E_2的诊断界值分别为96.245 ng/ml、2.383 ng/ml、0.028和105.293 pg/ml,其灵敏度和特异度分别为90.21%和45.22%、96.19%和51.07%、94.42%和56.69%、93.36%和40.71%。血清RANKL、OPG、OPG/RANKL比值和E_2均早于金标准出现阳性诊断结果。结论动态检测血清RANKL、OPG及E_2水平,有望实现运动性骨疲劳的早期预警。
基金supported by the grant of Key Program Foundation of Beijing TCMs Administration(2004-IV15),China
文摘Objective: To investigate the effects of anastrozole combined with Shuganjiangu decoction on osteoblast-like cells. Methods: Human osteoblast-like cells MG-63 were cultured and divided into four groups control, anastrozole, Shuganjiangu decoction (SGJGD), and anastrozole combined with SGJGD. Cell proliferation was investigated by M-IF assay. Alkaline phosphatase (ALP) and osteocalcin, the indicators of cell differentiation, were evaluated by p-nitrophenyl- phosphate method and radioimmunoassay, respectively. Gene expressions of ALP, osteocalcin, osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) were examined by real-time PCR. Results: As evidenced by MTT assay, cell proliferation of MG-63 was inhibited by anastrozole, but stimulated with treatment of SGJGD alone and combined with anastrozole (P〈O.01). Compared with control group, ALP activity was increased by the treatment of SGJGD alone and combined with anastrozole (P〈0.01). Also, osteocalcin secretion was enhanced with the treatment of SGJGD single and combination with anastrozole (P〈O.05). In the real-time PCR assay, gene expressions of ALP and osteocalcin were significantly increased (P〈0.01 for ALP, P〈0.05 for osteocalcin) by the treatment of SGJGD and anastrozole combined with SGJGD, but the expression of RANKL was decreased (P〈O.05). Moreover, anastrozole combined with SGJGD upregulated gene expression of OPG (P〈O.01). Conclusion: SGJGD may alleviate the injury effects of anastrozole on MG-63 cells through adjusting bone formation and resorption indicators.
文摘骨骼是一个动态组织,在生物的整个生命周期中不断地进行构建、吸收、重建,核因子(nucler factor,NF)κB受体活化因子(receptor activator of NF-κB,RANK)/NF-κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)/护骨素(osteoprotegerin,OPG)系统是调控这一过程的关键系统。RANK/RANKL/OPG属于肿瘤坏死因子及其受体超家族,三者通过调控破骨细胞的分化和活化来影响骨吸收和重建的过程。另外,免疫细胞也参与和调节RANK/RANKL的表达和分泌,而免疫细胞本身亦受到该系统的影响,因此,RANK/RANKL/OPG系统成为骨和免疫之间的重要关联。RANK/RANKL/OPG系统的失衡与多种骨代谢性疾病及免疫系统疾病引发的继发性骨病密切相关,该系统的发现为研究相关疾病的病理机制和治疗方法提供了基础。由此建立的抗RANKL疗法已经开始应用于临床试验和研究。此文对RANK/RANKL/OPG系统、系统相关疾病以及抗RANKL治疗的进展做一综述。