北京荣志海达生物科技有限公司
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025-86978335
所在地区：北京/海淀区
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品牌名称：
型号规格：
批准文号： 非器械产品
产品标签：总可溶性破骨细胞异化因子
产品卖点：新产品
销售渠道：医院
025-86978335
| 器械类别 | 二类医疗器械 | 科室 | 诊断相关科室 |
| 功能 | 检测试剂盒 | 标准目录 | 体外循环及血液处理设备 |
| 耗材类别 | 其他分类 | 进口 | |
| 家用与否 |
产品介绍：
【产品名称】
通用名称：阿狄科®总可溶性破骨细胞异化因子检测试剂盒（酶联免疫法）
英文名称：total/sRANKL
【包装规格】
96人份/盒
【预期用途】
用于血清和血浆中总 sRANKL(human) 的定量测定。仅供科研使用。
【背景知识】
RANKL（NF-kB 配体的受体激活剂，也称为骨保护素配体，OPGL），其细胞受体 RANK 及其清道夫受体骨保护素 (OPG) 已被确定为人体内在骨重塑电路中的关键成分。 RANKL 是 TNF（肿瘤坏死因子）家族的成员，是破骨细胞成熟的主要刺激因素，对它们的生存至关重要。因此，RANKL 表达的增加导致骨吸收和丢失。RANKL 由成骨细胞谱系和活化的 T 淋巴细胞产生，并激活其位于破骨细胞和树突状细胞上的特异性受体 RANK。
RANKL 的作用受 OPG 控制，OPG 分泌于各种组织中，作为可溶性内源性受体拮抗剂。
佩吉特病、良性和恶性骨肿瘤、绝经后骨质疏松症、类风湿性关节炎、骨转移和高钙血症的发病机制与 RANKL/OPG 的不平衡有关，可以通过添加 OPG 来调节 RANKL/OPG 平衡。
RANKL 已显示在鼠成骨细胞或基质细胞中作为膜结合蛋白表达，并被金属蛋白酶切割成可溶形式 (sRANKL)。TNFa 还促进 RANKL 的表达并抑制 OPG 在成骨细胞或基质细胞中的表达细胞因子如 IL-13、INF-g 和 TNF-α1，它们抑制破骨细胞生成，抑制 RANKL 的表达并刺激 OPG 的表达。
适应症：
绝经后和老年性骨质疏松症
局部骨吸收增加的疾病
佩吉特病
牙周病
炎症性疾病
免疫系统疾病
关节炎
肿瘤学
参考文献：
1. Lacey D.L, et al., Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.Cell (1998),93:165-176.
2. Kong Y.Y.et al., OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis.Nature (1999),397:315-323.
3. Hsu H.et al.,Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. Proc NatlAcad Sci (1999),96:3540-3545.
4. Josien R, et al, TRANCE, a tumor necrosis factor family member, enhances the longevity and adjuvant properties of dendritic cells in vivo.JExp Med (2000),191:495-502.
5. Fuller K.et al.,TRANCEis necessary and sufficient for osteoblast-mediated activation of bone resorption in osteoclasts. JExp Med (1998),188:997-1001.
6. Nakashima T , et. al., Protein expression and functional difference of membrane bound and soluble receptor activator of NF-kappaB ligand: modulation of theexpression by osteotropic factors and cytokines. Biochem Biophys Res Commun(2000), 275(3):768-75.
7. Kong Y.Y.et al,Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand.Nature (1999),402:304-309.
8. Hofbauer L.C.&A.E.Heufelder, Role of receptor activator of nuclear factor-KB ligand and osteoprotegerin in bone cell biology.J Mol Med (2001),79:243-253.
9. Hofbauer L.C.& A.E.Heufelder, The Role of Osteoprotegerin and Receptor Activator of Nuclear Factor KB Ligand in the Pathogenesis and Treatment of Rheumato-id Arthritis.Arthritis & Rheumatism (2001),44:253-259.
10.Hofbauer LC, et al...The role of receptor activator of nuclear factor-kappaB ligand and osteoprotegerin in the pathogenesis and treatment of metabolic bone di-seases.JCin Endocrinol metab (2000),85: 2355-2363.
11.Teitelbaum S.L., Bone resorption by osteoclasts.Science (2000), 289:1504-1508.
12.Boumans,M.J.H. et al., 2012.Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis.Annals of the rheumatic diseases,71(1),pp.108-13.
13. Dovio, A.et al., 2008.Circulating osteoprotegerin and soluble RANK ligand in systemic sclerosis.The Journal of rheumatology, 35(11), pp.2206-13.
14.Dovio, A.et al., 2007.Increased osteoprotegerin levels in Cushings syndrome are associated with an adverse cardiovascular risk profile.The Journal of clinical endo-crinology and metabolism,92(5),pp.1803-8.
15.Findlay, D. et al., 2008.Circulating RANKL is inversely related to RANKL mRNA levels in bone in osteoarthritic males.Arthritis research & therapy,10(1), p.R2.
16.Gonzélez-Alvaro, l.et al., 2007.baseline serum RANKL levels may serve to predict remission in rheumatoid arthritis patients treated with TNF antagonists.Annals ofthe rheumatic diseases, 66(12), pp.1675-8.
17.Hein, G. et al., 2000. vergleich der Serum- und Synovia-Spiegel von sRANKL und OPG bei rheumatoider Arthritis und nicht erosiven Arthritiden.Poster beim Kon-gress der Deutschen Gesellschaft fur Rheumatologie. Dresden.
18.Hein, G.E. et al.,2008. sRANKL and OPG in serum and synovial fluid of patients with rheumatoid arthritis in comparison to non-destructive chronic arthritis.Rheumatology international, 28(8), pp.765-9.
19.Hofbauer, L.C. et al., 2004.Effects of oral contraceptives on circulating osteoprotegerin and soluble RANK ligand serum levels in healthy young women.Clinicalendocrinology, 60(2).pp.214-9.
20.Kamiya,N. et al, 2011. Significance of serum osteoprotegerin and receptor activator of nuclear factor xB ligand in Japanese prostate cancer patients with bonemetastasis. lnternational journal of clinical oncology,16(4), pp.366-72.
21.Kerschan-Schindl, K. et al., 2008. Serum levels of receptor activator of nuclear fac-
tor kappaB ligand (RANKL) in healthy women and men.Experimental and clinicalendocrinology & diabetes : official journal, German Society of Endocrinology [and]German Diabetes Association, 116(8).pp.491-5.
22.Li, E.K. et al., 2009.High prevalence of asymptomatic vertebral fractures in Chinese women with systemic lupus erythematosus.The Journal of rheumatology,36(8), pp.1646-52.
23.Nielen, M. et al.，, 2004.Markers of bone formation and resorption in preclinical rheumatoid arthritis are associated with radiographic progression. Poster beimAmerican College of Rheumatology Meeting. San Diego.
24.Oelzner, P. et al., 2009.Beziehung zwischen loslichen Komponenten des IL-6-Systems und des RANKL-OPG-Systems bei postmenopausalen Frauen mit Rheuma-toider Arthritis.Poster bei Osteologie. Frankfurt.
25.Oelzner, P. et al., 2006.RANKL ，Osteoprotegerin und IlL-6-System bei Rheumatoider Arthritis -EinfluR von Alter ，Erkrankungsdauer , Menopause und entzund-licher Aktivitat.Poster bei Osteologie.Koln.
26.Schederl, J.et al., 2005.P148- Osteoprotegerin, RANK-Ligand und 5b-b TRAP bei Patienten mit Morbus Crohn.Zeitschrift fur Gastroenterologie, 43, p.812.
27.Secchiero, P. et al., 2006.An increased osteoprotegerin serum release characterizes the early onset of diabetes mellitus and may contribute to endothelial celldysfunction. The American journal of pathology,169(6), pp.2236-44.
