雌激素作用下罗格列酮对RAW264.7向破骨细胞分化的影响

doi:10.13701/j.cnki.kqyxyj.2019.05.021

口腔医学研究 ›› 2019, Vol. 35 ›› Issue (5): 502-506.DOI: 10.13701/j.cnki.kqyxyj.2019.05.021

• 口腔干细胞与口腔生物学研究 • 上一篇

雌激素作用下罗格列酮对RAW264.7向破骨细胞分化的影响

胡英英, 哈珊珊, 朱宁静, 宋亚玲, 汪昌宁^*

口腔基础医学省部共建国家重点实验室培育基地和口腔生物医学教育部重点实验室, 武汉大学口腔医学院湖北武汉 430079

收稿日期:2019-01-15 出版日期:2019-05-28 发布日期:2019-05-21
通讯作者: 汪昌宁, E-mail:wangcn@whu.edu.cn
作者简介:胡英英(1992~ ),女,江西九江人,硕士在读,主要从事牙周病学相关研究工作。
基金资助:
国家自然科学基金(编号:81670976)

Effect of Rosiglitazone on Osteoclastic Differentiation of RAW264.7 Cells under Estrogen.

HU Ying-ying, HA Shan-shan, ZHU Ning-jing, SONG Ya-ling, WANG Chang-ning^*

The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-Most) &Key Laboratory of Oral Biomedicine Ministry of Education, School &Hospital of Stomatology, Wuhan University, Wuhan 430079, China.;

Received:2019-01-15 Online:2019-05-28 Published:2019-05-21

摘要/Abstract

摘要： 目的: 研究雌激素作用下,罗格列酮对RAW264.7向破骨细胞分化的影响及机制。方法: 破骨细胞诱导液核因子-κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL)诱导鼠巨噬细胞系RAW264.7细胞,加入罗格列酮和/或雌激素诱导5 d,抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色检测破骨细胞数量,实时荧光定量聚合酶链反应(real-time fluorescent quantitative polymerase chain reaction,qRT-PCR)检测破骨相关基因和转录因子的表达;噻唑蓝(methyl thiazol tetrazolium,MTT)检测罗格列酮和/或雌激素对细胞活性影响。结果: RANKL诱导破骨细胞形成,且在罗格列酮或雌激素刺激下,破骨细胞数量增加,破骨相关基因和转录因子表达增高(P＜0.05);但在雌激素作用下罗格列酮抑制破骨细胞形成,破骨相关基因及转录因子表达显著降低(P＜0.05)。结论: 雌激素作用下罗格列酮可能通过肿瘤坏死因子受体相关因子6(tumor necrosis factor receptor associated factor 6,TRAF6)和活化T细胞核因子,细胞质1(nuclear factor of activated T-cells, cytoplasmic 1,NFATc1)抑制破骨细胞形成。

关键词: 过氧化物酶体增殖物激活受体γ, 罗格列酮, 雌激素, 破骨细胞

Abstract: Objective: To investigate the effect and mechanism of rosiglitazone on osteoclastic differentiation of RAW264.7 cells under estrogen. Methods: The murine macrophage RAW264.7 cells lines were induced by RANKL in the presence or absence of rosiglitazone and/or estrogen for 5 days. The number of osteoclasts was detected by TRAP staining and the expression of osteoclast related genes and transcription factors were detected by qRT-PCR. The effects of rosiglitazone and/or estrogen on cell viability were detected by MTT. Results: Rosiglitazone and estrogen increased cell viability. RANKL induced osteoclast formation and the number of osteoclasts, osteoclast related genes and translation factors increased under rosiglitazone or estrogen stimulation (P<0.05). However, rosiglitazone inhibited osteoclast formation, and osteoclast related genes and translation factors were significantly decreased under estrogen (P<0.05). Conclusion: Rosiglitazone could inhibit osteoclast formation by TRAF6 and NFATc1 under estrogen.

Key words: PPARγ, Rosiglitazone, Estrogen, Osteoclast

胡英英, 哈珊珊, 朱宁静, 宋亚玲, 汪昌宁. 雌激素作用下罗格列酮对RAW264.7向破骨细胞分化的影响[J]. 口腔医学研究, 2019, 35(5): 502-506.

HU Ying-ying, HA Shan-shan, ZHU Ning-jing, SONG Ya-ling, WANG Chang-ning. Effect of Rosiglitazone on Osteoclastic Differentiation of RAW264.7 Cells under Estrogen.[J]. Journal of Oral Science Research, 2019, 35(5): 502-506.

参考文献

[1] Wang Q, Yao L, Xu K, et al. Madecassoside inhibits estrogen deficiency-induced osteoporosis by suppressing RANKL-induced osteoclastogenesis [J]. J Cell Mol Med, 2019, 23(1):380-394.
[2] Wei W, Wang X, Yang M, et al. PGC1beta mediates PPARgamma activation of osteoclastogenesis and rosiglitazone-induced bone loss [J]. Cell Metab, 2010, 11(6):503-516.
[3] Humphrey MB, Nakamura MC. A comprehensive review of immunoreceptor regulation of osteoclasts [J]. Clin Rev Allergy Immunol, 2016, 51(1):48-58.
[4] Xin Z, Jin C, Chao L, et al. A matrine derivative M54 suppresses osteoclastogenesis and prevents ovariectomy-induced bone loss by targeting ribosomal protein S5 [J]. Front Pharmacol, 2018, 9:22.
[5] Reddy MS, Morgan SL. Decreased bone mineral density and periodontal management [J]. Periodontol 2000, 2013, 61(1):195-218.
[6] 杨芳,陈明月,胡英英,等.PPARγ在脂多糖刺激牙周膜细胞中调控NF-κB信号通路的作用研究[J].口腔医学研究,2017,33(7):698-702.
[7] Kahn SE, Zinman B, Lachin JM, et al. Rosiglitazone-associated fractures in type 2 diabetes: an analysis from a diabetes outcome progression trial (ADOPT) [J]. Diabetes Care, 2018, 31(5):845-851.
[8] Lazarenko OP, Rzonca SO, Hogue WR, et al. Rosiglitazone induces decreases in bone mass and strength that are reminiscent of aged bone [J]. Endocrinology, 2007, 148(6):2669-2680.
[9] Case N, Thomas J, Xie Z, et al. Mechanical input restrains PPARgamma2 expression and action to preserve mesenchymal stem cell multipotentiality [J]. Bone, 2013, 52(1):454-464.
[10] Koufany M, Chappard D, Netter P, et al. The peroxisome proliferator-activated receptor gamma agonist pioglitazone preserves bone microarchitecture in experimental arthritis by reducing the interleukin-17-dependent osteoclastogenic pathway [J]. Arthritis Rheum, 2013, 65(12):3084-3095.
[11] Qiao W, Wang C, Huang W, et al. Peroxisome proliferator-activated receptor gamma plays dual roles on experimental periodontitis in rats [J]. J Clin Periodontol, 2018, 45(5):514-523.
[12] Yan DJ, Chen ZW. 17beta-estradiol increased the expression of daintain/AIF-1 in RAW264.7 macrophages [J]. Biosci Biotechnol Biochem, 2010, 74(10):2103-2105.
[13] Guo L, Chen K, Yuan J, et al. Estrogen inhibits osteoclasts formation and bone resorption via microRNA-27a targeting PPARgamma and APC [J]. J Cell Physiol, 2018, 234(1):581-594.
[14] Chen F, Ouyang Y, Ye T, et al. Estrogen inhibits RANKL-induced osteoclastic differentiation by increasing the expression of TRPV5 channel [J]. J Cell Biochem, 2014, 115(4):651-658.
[15] Schwartz AV, Sellmeyer DE, Vittinghoff E. Thiazolidinedione use and bone loss in older diabetic adults [J]. J Clin Endocrinol Metab, 2006, 91(9):3349-3354.
[16] Nakaya M, Tachibana H, Yamada K. Isoflavone genistein and daidzein up-regulate LPS-induced inducible nitric oxide synthase activity through estrogen receptor pathway in RAW264.7 cells [J]. Biochem Pharmacol, 2005, 71(1-2):108-114.
[17] Wu J, Ru N, Li S. Peroxisome proliferator-activated receptor gamma regulates bone remodeling after midpalatal suture expansion in mice [J]. Int J Oral Maxillofac Implants, 2015, 30(6):1423-1430.
[18] You HJ, Kim JY, Jeong HG. 17β-Estradiol increases inducible nitric oxide synthase expression in macrophages [J]. Biochem Biophys Res Commun, 2003, 303(4):1129-1134.
[19] Powell B, Szleifer I, Dhaher YY. In silico study of principal sex hormone effects on post-injury synovial inflammatory response [J]. PLoS One, 2018, 13(12):e0209582.
[20] Fan P, Abderrahman B, Chai TS, et al. Targeting peroxisome proliferator-activated receptor gamma to increase estrogen-induced apoptosis in estrogen-deprived breast cancer cells [J]. Mol Cancer Ther, 2018, 17(12):2732-2745.
[21] Peng X, Qiao Z, Wang Y, et al. Estrogen reverses nicotine-induced inflammation in chondrocytes via reducing the degradation of ECM [J]. Int J Rheum Dis, 2019, 22(4):666-676.
[22] Yang Y, Zhang N, Lan F, et al. Transforming growth factor-beta 1 pathways in inflammatory airway diseases [J]. Allergy, 2014, 69(6):699-707.
[23] Li Z, Zhang W, Huang Y. MiRNA-133a is involved in the regulation of postmenopausal osteoporosis through promoting osteoclast differentiation [J]. Acta Biochim Biophys Sin (Shanghai), 2018, 50:273-280.
[24] Pi Y, Liang H, Yu Q, et al. Lowfrequency pulsed electromagnetic field inhibits RANK Linduced osteoclastic differentiation in RAW264.7 cells by scavenging reactive oxygen species[J]. Mol Med Rep, 2019, 19(5):4129-4136.
[25] Wang J, Wu X, Duan Y. Magnesium lithospermate B protects against lipopolysaccharide-induced bone loss by inhibiting RANKL/RANK pathway [J]. Front Pharmacol, 2018, 9:64.
[26] Yao Z, Lei W, Duan R, et al. RANKL cytokine enhances TNF-induced osteoclastogenesis independently of TNF receptor associated factor (TRAF) 6 by degrading TRAF3 in osteoclast precursors [J]. J Biol Chem, 2017, 292(24):10169-10179.

雌激素作用下罗格列酮对RAW264.7向破骨细胞分化的影响

Effect of Rosiglitazone on Osteoclastic Differentiation of RAW264.7 Cells under Estrogen.

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