| [1] Levinger I, Seeman E, Jerums G, et al. Glucose-loading reduces bone remodeling in women and osteoblast function in vitro. Physiol Rep. 2016;4(3). pii: e12700. [2] Cheng SL, Zhang SF, Avioli LV. Expression of bone matrix proteins during dexamethasone-induced mineralization of human bone marrow stromal cells. J Cell Biochem. 1996; 61(2):182-193.[3] Iba K, Chiba H, Sawada N,et al. Glucocorticoids induce mineralization coupled with bone protein expression without influence on growth of a human osteoblastic cell line.Cell Struct Funct. 1995;20(5):319-330.[4] Weinstein RS, Jilka RL, Parfitt AM,et al.Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone. J Clin Invest. 1998;102(2): 274-282. [5] Hirayama T, Sabokbar A, Athanasou NA. Effect of corticosteroids on human osteoclast formation and activity. The Journal of endocrinology. 2002;175(1):155-63.[6] Stewart PM, Krozowski ZS. 11 beta-Hydroxysteroid dehydrogenase. Vitam Horm. 1999;57:249-324. [7] Yang K, Smith CL, Dales D,et al. Cloning of an ovine 11 beta-hydroxysteroid dehydrogenase complementary deoxyribonucleic acid: tissue and temporal distribution of its messenger ribonucleic acid during fetal and neonatal development. Endocrinology. 1992;131(5):2120-6.[8] Brown RW, Chapman KE, Kotelevtsev Y, et al.Cloning and production of antisera to human placental 11β-hydroxysteroid dehydrogenase type 2. Biochem J. 1996;313(Pt 3): 1007-1017.[9] Bland R, Worker CA, Noble BS, et al. Characterization of 11β-hydroxysteroid dehydrogenase activity and corticosteroid receptor expression in human osteosarcoma cell lines. J Endocrinol. 1999;161(3):455-464.[10] Condon J, Gosden C, Gardener D, et al.Expression of Type 2 11 -Hydroxysteroid Dehydrogenase and Corticosteroid Hormone Receptors in Early Human Fetal Life.J Clin Endocrinol Metab. 1998;83(12):4490-4497.[11] 赵佳,魏波,刘军,等. 皮质酮对大鼠股骨头微环境11β-HSD1表达及骨重建影响的初步实验研究[J]. 重庆医学. 2016,45(3): 336-338.[12] Cooper MS, Blumsohn A, Goddard PE,et al. 11beta-hydroxysteroid dehydrogenase type 1 activity predicts the effects of glucocorticoids on bone. J Clin Endocrinol Metab. 2003;88(8):3874-3877.[13] Chiodini I, Carnevale V, Torlontano M, et al. Alterations of Bone Turnover and Bone Mass at Different Skeletal Sites due to Pure Glucocorticoid Excess: Studyin Eumenorrheic Patients with Cushing’s Syndrome. J Clin Endocrinol Metab. 1998;83(6):1863-1867.[14] Dennison E, Hindmarsh P, Fall C, et al. Profiles of Endogenous Circulating Cortisol and Bone Mineral Density in Healthy Elderly Men*. J Clin Endocrinol Metab.1999;84: 3058-3063.[15] Huizenga NA, Koper JW, De Lange P,et al. A Polymorphism in the Glucocorticoid Receptor Gene May Be Associated with an Increased Sensitivity to Glucocorticoids in Vivo. J Clin Endocrinol Metab. 1998;83(1):144-151.[16] Kaji H, Sugimoto T, Kanatani M, et al. Dexamethasone stimulates osteoclast-like cell formation by directly acting on hemopoietic blast cells and enhances osteoclast-like cell formation stimulated by parathyroid hormone and prostaglandin E2. J Bone Miner Res.1997;12(5):734-741.[17] Cooper MS, Walker EA, Bland R, et al. Expression and Functional Consequences of 11β-Hydroxysteroid Dehydrogenase Activity in Human Bone. Bone.2000;27: 375-381.[18] Park JS, Bae SJ, Choi SW, et al. A novel 11βHSD1 inhibitor improves diabesity and osteoblast Differentiation. J Mol Endocrinol. 2014 ;52(2):191-202.[19] Eijken M,Hewison M,Cooper MS,et al.11beta-Hydroxysteroid dehydrogenase expression and glucocorticoid synthesis are directed by a molecular switch during osteoblast differentiation. Mol Endocrinol. 2005;19(3):621-631.[20] Ramli ES, Suhaimi F, Asri SF, et al. Glycyrrhizic acid (GCA) as 11beta-hydroxysteroid dehydrogenase inhibitor exerts protective effect against glucocorticoid-induced osteoporosis. J Bone Miner Metab. 2013;31(3):262-273.[21] Cooper MS , Rabbitt EH , Goddard PE，et al.Osteoblastic 11 -Hydroxysteroid Dehydrogenase Type 1Activity Increases With Age and Glucocorticoid Exposure. J Bone Miner Res 2002;17 (6): 979-86.[22] Haynesworth SE, Goshima J, Goldberg VM,et al.Characterization of cells with osteogenic potential from human marrow. Bone.1992;13(1):81-88.[23] Herbertson A, Aubin JE.Dexamethasone alters the subpopulation make-up of rat bone marrow stromal cell cultures.J Bone Miner Res.1995;10(2):285-294.[24] Zhou H, Mak W, Kalak R,et al.Glucocorticoid-dependent Wnt signaling by mature osteoblastsis a key regulator of cranial skeletal development in mice. Development.2009;136(3):427-436.[25] Van Staa TP, Leufkens HG, Abenhaim L,et al. Use of oral corticosteroids and risk of fractures. June, 2000.J Bone Miner Res. 2005 ;20(8):1487-494.[26] Canalis E. Clinical review 83: Mechanisms of glucocorticoid action in bone: implications to glucocorticoid-induced osteoporosis. J Clin Endocrinol Metab. 1996;81(10): 3441-3447 [27] Brockstedt H, Kassem M, Eriksen EF,et al.Age- and sex-related changes in iliac cortical bone mass and remodeling. Bone.1993,14(4):681-691.[28] Clarke BL, Ebeling PR, Jones JD,et al.Changes in quantitative bone histomorphometry in aging healthy men. J Clin Endocrinol Metab. 1996;81(6):2264-2270.[29] Hardy RS, Raza K, Cooper MS. Glucocorticoid metabolism in rheumatoid arthritis. Ann N Y Acad Sci. 2014;1318:18-26. [30] Hardy R,Rabbitt EH,Filer A,et al.Local and systemic glucocorticoid metabolism in inflammatory arthritis. Ann Rheum Dis. 2008;67(9):1204-1210. [31] 徐杰,李国平,唐蔚青,等. I型11β羟基类固醇脱氢酶在肿瘤坏死因子-α诱导的胰岛素抵抗中的作用[J]. 中年老年医学杂志. 2016,35(5): 537-542.[32] Cai TQ, Wong B, Mundt SS, et al. Induction of 11beta-hydroxysteroid dehydrogenase type 1 but not -2 in human aortic smooth muscle cells by inflammatory stimuli. J Steroid Biochem Mol Biol. 2001;77(2-3):117-22.[33] Escher G, Galli I, Vishwanath BS, et al. Tumor Necrosis Factorа Interleukin1βEnhance the Cortisone/Cortisol Shuttle. J Exp Med. 1997;186(2):189-198.[34] Kaur K,Hardy R,Ahasan MM,et al.Synergistic induction of local glucocorticoid generation by inflammatory cytokines and glucocorticoids: implications for inflammation associated bone loss. Ann Rheum Dis. 2010;69(6):1185-1190.[35] Brabnikova Maresova K, Pavelka K, Stepan JJ.Acute effects of glucocorticoids on serum markers of osteoclasts, osteoblasts, and osteocytes. Calcif Tissue Int. 2013;92(4): 354-361. [36] Wang FS, Ko JY, Yeh DW, et al. Modulation of Dickkopf-1 Attenuates Glucocorticoid Induction of Osteoblast Apoptosis, Adipocytic Differentiation, and Bone Mass Loss. Endocrinology. 2008;149(4):1793-801.[37] Cooper MS, Bujalska I, Rabbitt E, et al. Modulation of 11beta-hydroxysteroid dehydrogenase isozymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation. J Bone Miner Res. 2001 ;16(6):1037-1044. [38] Kostadinova RM, Nawrocki AR, Frey FJ, et al. Tumor necrosis factor alpha and phorbol 12-myristate-13-acetate down-regulate human 11beta-hydroxysteroid dehydrogenase type 2 through p50/p50 NF-kappaB homodimers and Egr-1. FASEB J. 2005;19(6):650-652.[39] Li F, Qiao C, Li Y, et al. Blockade of 11β-hydroxysteroid dehydrogenase type 1 enzyme inhibits experimental collagenase-induced osteoarthritis. Mol Med Rep. 2015;11(3): 2071-2075.[40] Doig CL, Bashir J, Zielinska AE, et al. TNFa-mediated Hsd11b1 binding of NF-kB p65 is associated with suppression of 11b-HSD1 in muscle. J Endocrinol. 2014;220(3):389-396.[41] Nakano D, Nishiyama A. Programmed 11beta-hydroxysteroid dehydrogenase type 2 reduction: a possible cause of adult-onset disease?. J Hypertens. 2011;29(2):201-203.[42] Kerachian MA, Seguin C, Harvey EJ. Glucocorticoids in osteonecrosis of the femoral head: a new understanding of the mechanisms of action.J Steroid Biochem Mol Biol.2009; 114(3-5):121-128.[43] 李璐,辛婧,薛一,等. 11-HSD1与S100A16共同调节3T3-L1脂肪细胞的分化[J]. 中华内分泌代谢杂志，2014,30(9):779-85.[44] Wang L,Luo DK,Pan ZY.Expression of 11beta-HSD in steroid-induced avascular necrosis of the femoral head. Mol Med Rep.2013;7(5):1482-1486.[45] 李玉英, 王陈钱.地塞米松对血管内皮细胞11-HSD1基因表达的影响[J]. 解放军医学杂志,2007,32(10):1066-1068. |
.jpg)
文题释义：
骨特异性碱性磷酸酶：是骨生长过程中持续释放时间最长的细胞因子，并且还具有组织特异性强、时间变异性小的特点。其由成骨细胞产生，是碱性磷酸酶的亚型，存在于成骨细胞膜结合物。骨特异性碱性磷酸酶是反映骨形成和成骨细胞活性的敏感和特异指标，能排除肝、肾、肠等疾病影响，是成骨细胞的胞外酶，成骨细胞活性增强，则骨特异性碱性磷酸酶分泌增加。
骨代谢：骨不断地进行着重建，骨重建过程包括破骨细胞贴附在旧骨区域，分泌酸性物质溶解矿物质，分泌蛋白酶消化骨基质，形成骨吸收陷窝；其后，成骨细胞移行至被吸收部位，分泌骨基质，骨基质矿化而形成新骨。破骨与成骨过程的平衡是维持正常骨量的关键。
.jpg)
.jpg)
文题释义：
骨特异性碱性磷酸酶：是骨生长过程中持续释放时间最长的细胞因子，并且还具有组织特异性强、时间变异性小的特点。其由成骨细胞产生，是碱性磷酸酶的亚型，存在于成骨细胞膜结合物。骨特异性碱性磷酸酶是反映骨形成和成骨细胞活性的敏感和特异指标，能排除肝、肾、肠等疾病影响，是成骨细胞的胞外酶，成骨细胞活性增强，则骨特异性碱性磷酸酶分泌增加。
骨代谢：骨不断地进行着重建，骨重建过程包括破骨细胞贴附在旧骨区域，分泌酸性物质溶解矿物质，分泌蛋白酶消化骨基质，形成骨吸收陷窝；其后，成骨细胞移行至被吸收部位，分泌骨基质，骨基质矿化而形成新骨。破骨与成骨过程的平衡是维持正常骨量的关键。