[1] Findlay DM.If good things come from above, do bad things come from below? Arthritis Res Ther. 2010;12(3):119.[2] Bijlsma JW, Berenbaum F, Lafeber FP. Osteoarthritis: an update with relevance for clinical practice. The Lancet. Lancet. 2011;377(9783):2115-2126.[3] 贾云柱,史松林.口服氨基葡萄糖配合臭氧与玻璃酸钠关节腔注射治疗膝骨关节炎90例[J]. 中国组织工程研究, 2015,19(增刊): 68-70.[4] 邱贵兴,翁习生,盐酸/硫酸氨基葡萄糖治疗骨关节炎的平行对照临床研究[J].中华医学杂志,2005;85(43):3067-3070.[5] 施桂英,骨关节炎及其药物治疗的最佳选择[J].中华风湿病学杂志,2003.7(3):129-132.[6] 中华医学会风湿病学分会,骨关节炎诊断及治疗指南[J].中华风湿病学杂志,2010.14(6):416-419.[7] Martinon F, Mayor A, Tschopp J. The inflammasomes: guardians of the body. Annu Rev Immunol. 2009;27: 229-265.[8] Muñoz-Planillo R, Kuffa P, Martínez-Colón G,et al.K(+) efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity. 2013; 38(6): 1142-1153.[9] 张照庆,熊彭.改良伸直位固定法建立兔膝骨性关节炎模型的研究[J]. 湖北中医学院学报, 2010,12(5): 19-21.[10] Mankin HJ, Dorfman H, Lippiello L,et al.Biochemical and Metabolic Abnormalities in Articular Cartilage from Osteo-Arthritic Human Hips. J Bone Joint Surg Am. 1971; 53(3):523-537. [11] 许良中,杨文涛, 免疫组织化学反应结果的判断标准[J]. 中国癌症杂志, 1996,6(4): 229-231.[12] 张洪, 关节制动制作骨性关节炎动物模型的探讨[J]. 中国现代医学杂志,2006,16(12):1843-1848.[13] 何明江,张洪美,荆琳.骨关节炎动物模型:谁最适宜你的研究?[J].中国组织工程研究, 2013,17(64): 8075.[14] Pers YM, Rackwitz L, Ferreira R,et al.Adipose Mesenchymal Stromal Cell-Based Therapy for Severe Osteoarthritis of the Knee: A Phase I Dose-Escalation Trial. Stem Cells Transl Med. 2016;5(7): 847-856.[15] Nakajima M,Miyamoto Y,Ikegaw a S.Cloning andcharacterization of the osteoarthritis associated gene DVWA. J Bone Miner Metab.2011;29(3):300-308.[16] 袁芳,何晓瑾.骨关节炎的软骨凋亡机制[J].实用医学,2015,31(4): 666-668.[17] de Vasconcelos NM, Van Opdenbosch N, Lamkanfi M.Inflammasomes as polyvalent cell death platforms. Cell Mol Life Sci.Cell Mol Life Sci.2016;73(11-12):2335-2347. [18] Finger JN, Lich JD, Dare LC,et al.Autolytic Proteolysis within the Function to Find Domain (FIIND) Is Required for NLRP1 Inflammasome Activity.J Biol Chem. 2012;287(30): 25030-25037. [19] McCall SH,Sahraei M,Young AB,et al.Osteoblasts express NLRP3, a nucleotide-binding domain and leucine-rich repeat region containing receptor implicated in bacterially induced cell death. J Bone Miner Res.2008;23(1): 30-40.[20] Chen ZH, Jin SH, Wang MY,et al.Enhanced NLRP3, caspase-1, and IL- 1beta levels in degenerate human intervertebral disc and their association with the grades of disc degeneration. Anat Rec (Hoboken).2015;298(4): 720-726.[21] 王海南,刘殷.白介素-1在骨关节炎发病机制中的研究进展[J]. 中国骨伤, 2012, 25(2): 175-178.[22] 祁会丽.细胞焦亡激活机制及相关疾病研究进展[J].中华实验诊断与治疗, 2016. 30(5):417-419.[23] Vande Walle L, Van Opdenbosch N, Jacques P, et al.Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis. Nature.2014;512(7512):69-73.[24] 吴小山,陈飞虎,胞外酸化对大鼠关节软骨细胞焦亡的影响及可能机制[J].中国药理学通报,2016Nov;32(11):1531-1539[25] Shi J, Zhao Y, Wang K, et al.Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature.2015;526(7575): 660-665.[26] Sborgi L, Rühl S, Mulvihill E, et al.GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death. EMBO J.2016;35(16):1766-1778. |