白细胞介素-1?在骨关节炎发生机制中作用的研究进展
摘要
<正>骨关节炎(osteoarthritis,OA)是中老年人常见的慢性关节疾病,病理特点为关节软骨退行性改变、破坏及继发性软骨下骨质增生,临床上表现为关节疼痛、畸形、功能障碍等,严重影响患者生活质量[1]。OA的发病机制尚不明确,一般认为与患者的年龄、性别、肥胖、关节创伤及过度使用、内分泌代谢障碍、遗传易感性等有关,是多因素相互作用的结果[2]。近年来细胞因子在OA发病机制中的作用越来越受人们的关注。研究发现,白细胞介素-1(interleukin-1,IL-1)生物学作用广泛,局部及全身均可以发挥作用,参与炎症反应,促使软骨组织损
引文
[1]Hinman RS,Crossley KM.Patellofemoral joint osteoarthritis:An important subgroup of knee osteoarthritis.Rheumatology(Oxford,Eng-land),2007,7:1057-1062.
[2]Felson DT.Osteoarthritis:new insights.Part 1:the disease and itsrisk factors.Ann Intern Med,2000,8:635-646.
[3]Santangelo KS,Nuovo GJ,Bertone AL.In vivo reduction or blockade of interleukin-1βin primary osteoarthritis influences expression of mediators implicated in pathogenesis.Osteoarthritis Cartilage,2012,12:1610-1618.
[4]Calich AL,Domiciano DS,Fuller R.Osteoarthritis:can anti-cytokine therapy play a role in treatment?Clin Rheumatol,2010,29:451-455.
[5]熊伟,夏仁云.IL-1家族及其受体与骨关节炎.中国矫形外科杂志,2003,5:337-338.
[6]Schepens SL,Kratz AL,Murphy SL.Fatigability in osteoarthritis:effects of an activity bout on subsequent symptoms and activity.J Gerontol A Biol Sci Med Sci,2012,10:1114-1120.
[7]Rannou F,Sellam J,Berenbaum F.Pathophysiology of osteoarthritis:updated concepts.Presse Med,2010,39:1159-1163.
[8]Murray DH,Bush PG,Brenkel IJ,et al.Abnormal human chondrocyte morphology is related to increased levels of cell associated IL-1βand disruption to pericellular collagen type VI.J Orthop Res,2010,11:1507-1514.
[9]Marks PH,Donaldson ML.Inflammatory cytokine profiles associated with chondral damage in the anterior cruciate ligament-deficient knee.Arthroscopy,2005,11:1342-1347.
[10]Stoddart MJ,Grad S,Eglin D,et al.Cells and biomaterials in cartilage tissue engineering.Regen Med,2009,1:81-89.
[11]Suzuki M,Hashizume M,Yoshida H,et al.IL-6 and IL-1 synergistically enhanced the production of MMPs from synovial cells by up-regulating IL-6 production and IL-1 receptor I expression.Cytokine,2010,2:178-183.
[12]Wang X,Li F,Fan C,et al.Effects and relationship of ERK1 and ERK2 in interleukin-1β-induced alterations in MMP3,MMP13,typeⅡcollagen and aggrecan expression in human chondrocytes.Int J Mol Med,2011,4:583-589.
[13]Abramson SB.Nitric oxide in inflammation and pain associated with osteoarthritis.Arthritis Res Ther,2008,2:S2.
[14]Héraud F,Héraud A,Harmand MF.Apoptosis in normal and osteoarthritic human articular cartilage.Ann Rheum Dis,2000,12:959-965.
[15]L'Hermette MF,Tourny-Chollet C,Polle G,et al.Articular cartilage,degenerative process,and repair:current progress.Int J Sports Med,2006,27:738-744.
[16]Palmieri B,Lodi D,Capone S.Osteoarthritis and degenerative joint disease:local treatment options update.Acta Biomed,2010,81:94-100.
[17]Elshaier AM,Hakimiyan AA,Rappoport L,et al.Effect of interleukin-1beta on osteogenic protein 1-induced signaling in adult human articular chondrocytes.Arthritis Rheum,2009,60:143-154.
[18]江建明,梁鹏展,刘传芳,等.转化生长因子β对白介素-1β诱导人骨关节炎软骨细胞表达NO的影响.中国骨与关节外科,2008,1:35-39.
[19]Davies CM,Guilak F,Weinberg JB,et al.Reactive nitrogen and oxygen species in interleukin-1-mediated DNA damage associated with osteoarthritis.Osteoarthritis Cartilage,2008,5:624-630.
[20]Kim J,Xu M,Xo R,et al.Mitochondrial DNA damage is involved in apoptosis caused by pro-inflammatory cytokines in human OA chondrocytes.Osteoarthritis Cartilage,2010,3:424-432.
[21]Dai SM,Shan ZZ,Nakamura H,et al.Catabolic stress induces features of chondrocyte senescence through overexpression of caveolin 1:possible involvement of caveolin 1-induced down-regulation of articular chondrocytes in the pathogenesis of osteoarthritis.Arthritis Rheum,2006,3:818-831.
[22]Rai PK,Singh AK,Singh OP,et al.Efficacy of leech therapy in the management of osteoarthritis(Sandhivata).Ayu,2011,32:213-217.
[23]García-Arnandis I,Guillén MI,Gomar F,et al.High mobility group box 1potentiates the pro-inflammatory effects of interleukin-1βin osteoarthritic synoviocytes.Arthritis Res Ther,2010,12:R165.
[24]Wassilew GI,Lehnigk U,Duda GN,et al.The expression of proinflammatory cytokines and matrix metalloproteinases in the synovial membranes of patients with osteroarthritis compared with traumatic knee disorders.Arthroscopy,2010,8:1096-1104.
[25]Kamm JL,Nixon AJ,Witte TH.Cytokine and catabolic enzyme expression in synovium,synovial fluid and articular cartilage of naturally osteoarthritic equine carpi.Equine Vet J,2010,8:693-699.
[26]邵俊杰,张先龙,蒋垚.IL-1在骨关节炎发病机制中的作用及相关基因治疗.国际骨科学杂志,2007,5:309-311.
[27]Wuertz K,Vo N,Kletsas D,et al.Inflammatory and catabolic signalling in intervertebral discs:the roles of NF-κB and MAP kinases.Eur Cell Mater,2012,23:103-119.
[28]Lee HS,Lee CH,Tsai HC,et al.Inhibition of cyclooxygenase 2expression by diallyl sulfide on joint inflammation induced by urate crystal and IL-1beta.Osteoarthritis Cartilage,2009,1:91-99.
[29]Raymond L,Eck S,Hays E,et al.RelA is required for IL-1beta stimulation of Matrix Metalloproteinase-1 ex-pression in chondrocytes.Osteoarthritis Cartilage,2007,4:431-441.
[30]Wuertz K,Vo N,Kletsas D,et al.Inflammatory and catabolic signalling in intervertebral discs:the roles of NF-κB and MAP kinases.Eur Cell Mater,2012,23:103-119.
[31]杜国庆,丁道芳,李玲慧,等.骨关节炎软骨退变基因调控的研究进展.中国矫形外科杂志,2013,11:1089-1093.
[32]Kimura H,Yukitake H,Suzuki H,et al.The chondroprotective agent ITZ-1 inhibits interleukin-1beta-induced matrix metalloproteinase-13production and suppresses nitric oxide-induced chondrocyte death.J Pharmacol Sci,2009,2:201-211.
[33]Radons J,Bosserhoff AK,Grssel S,et al.p38MAPK mediates IL-1-induced down-regulation of aggrecan gene expression in human chondrocytes.Int J Mol Med,2006,4:661-668.
[34]Sondergaard BC,Schultz N,Madsen SH,et al.MAPKs are essential upstream signaling pathways in prote-olytic cartilage degradation-divergence in pathways leading to aggrecanase and MMP-mediated articular cartilage degradation.Osteoarthritis Cartilage,2010,3:279-288.
[35]Fahmi H,Martel-pelletier J,Pelletier JP,et al.Peroxisome proliferatoractivated receptor gamma in osteoarthritis.Mod Rheumatol,2011,1:1-9.
[2]Felson DT.Osteoarthritis:new insights.Part 1:the disease and itsrisk factors.Ann Intern Med,2000,8:635-646.
[3]Santangelo KS,Nuovo GJ,Bertone AL.In vivo reduction or blockade of interleukin-1βin primary osteoarthritis influences expression of mediators implicated in pathogenesis.Osteoarthritis Cartilage,2012,12:1610-1618.
[4]Calich AL,Domiciano DS,Fuller R.Osteoarthritis:can anti-cytokine therapy play a role in treatment?Clin Rheumatol,2010,29:451-455.
[5]熊伟,夏仁云.IL-1家族及其受体与骨关节炎.中国矫形外科杂志,2003,5:337-338.
[6]Schepens SL,Kratz AL,Murphy SL.Fatigability in osteoarthritis:effects of an activity bout on subsequent symptoms and activity.J Gerontol A Biol Sci Med Sci,2012,10:1114-1120.
[7]Rannou F,Sellam J,Berenbaum F.Pathophysiology of osteoarthritis:updated concepts.Presse Med,2010,39:1159-1163.
[8]Murray DH,Bush PG,Brenkel IJ,et al.Abnormal human chondrocyte morphology is related to increased levels of cell associated IL-1βand disruption to pericellular collagen type VI.J Orthop Res,2010,11:1507-1514.
[9]Marks PH,Donaldson ML.Inflammatory cytokine profiles associated with chondral damage in the anterior cruciate ligament-deficient knee.Arthroscopy,2005,11:1342-1347.
[10]Stoddart MJ,Grad S,Eglin D,et al.Cells and biomaterials in cartilage tissue engineering.Regen Med,2009,1:81-89.
[11]Suzuki M,Hashizume M,Yoshida H,et al.IL-6 and IL-1 synergistically enhanced the production of MMPs from synovial cells by up-regulating IL-6 production and IL-1 receptor I expression.Cytokine,2010,2:178-183.
[12]Wang X,Li F,Fan C,et al.Effects and relationship of ERK1 and ERK2 in interleukin-1β-induced alterations in MMP3,MMP13,typeⅡcollagen and aggrecan expression in human chondrocytes.Int J Mol Med,2011,4:583-589.
[13]Abramson SB.Nitric oxide in inflammation and pain associated with osteoarthritis.Arthritis Res Ther,2008,2:S2.
[14]Héraud F,Héraud A,Harmand MF.Apoptosis in normal and osteoarthritic human articular cartilage.Ann Rheum Dis,2000,12:959-965.
[15]L'Hermette MF,Tourny-Chollet C,Polle G,et al.Articular cartilage,degenerative process,and repair:current progress.Int J Sports Med,2006,27:738-744.
[16]Palmieri B,Lodi D,Capone S.Osteoarthritis and degenerative joint disease:local treatment options update.Acta Biomed,2010,81:94-100.
[17]Elshaier AM,Hakimiyan AA,Rappoport L,et al.Effect of interleukin-1beta on osteogenic protein 1-induced signaling in adult human articular chondrocytes.Arthritis Rheum,2009,60:143-154.
[18]江建明,梁鹏展,刘传芳,等.转化生长因子β对白介素-1β诱导人骨关节炎软骨细胞表达NO的影响.中国骨与关节外科,2008,1:35-39.
[19]Davies CM,Guilak F,Weinberg JB,et al.Reactive nitrogen and oxygen species in interleukin-1-mediated DNA damage associated with osteoarthritis.Osteoarthritis Cartilage,2008,5:624-630.
[20]Kim J,Xu M,Xo R,et al.Mitochondrial DNA damage is involved in apoptosis caused by pro-inflammatory cytokines in human OA chondrocytes.Osteoarthritis Cartilage,2010,3:424-432.
[21]Dai SM,Shan ZZ,Nakamura H,et al.Catabolic stress induces features of chondrocyte senescence through overexpression of caveolin 1:possible involvement of caveolin 1-induced down-regulation of articular chondrocytes in the pathogenesis of osteoarthritis.Arthritis Rheum,2006,3:818-831.
[22]Rai PK,Singh AK,Singh OP,et al.Efficacy of leech therapy in the management of osteoarthritis(Sandhivata).Ayu,2011,32:213-217.
[23]García-Arnandis I,Guillén MI,Gomar F,et al.High mobility group box 1potentiates the pro-inflammatory effects of interleukin-1βin osteoarthritic synoviocytes.Arthritis Res Ther,2010,12:R165.
[24]Wassilew GI,Lehnigk U,Duda GN,et al.The expression of proinflammatory cytokines and matrix metalloproteinases in the synovial membranes of patients with osteroarthritis compared with traumatic knee disorders.Arthroscopy,2010,8:1096-1104.
[25]Kamm JL,Nixon AJ,Witte TH.Cytokine and catabolic enzyme expression in synovium,synovial fluid and articular cartilage of naturally osteoarthritic equine carpi.Equine Vet J,2010,8:693-699.
[26]邵俊杰,张先龙,蒋垚.IL-1在骨关节炎发病机制中的作用及相关基因治疗.国际骨科学杂志,2007,5:309-311.
[27]Wuertz K,Vo N,Kletsas D,et al.Inflammatory and catabolic signalling in intervertebral discs:the roles of NF-κB and MAP kinases.Eur Cell Mater,2012,23:103-119.
[28]Lee HS,Lee CH,Tsai HC,et al.Inhibition of cyclooxygenase 2expression by diallyl sulfide on joint inflammation induced by urate crystal and IL-1beta.Osteoarthritis Cartilage,2009,1:91-99.
[29]Raymond L,Eck S,Hays E,et al.RelA is required for IL-1beta stimulation of Matrix Metalloproteinase-1 ex-pression in chondrocytes.Osteoarthritis Cartilage,2007,4:431-441.
[30]Wuertz K,Vo N,Kletsas D,et al.Inflammatory and catabolic signalling in intervertebral discs:the roles of NF-κB and MAP kinases.Eur Cell Mater,2012,23:103-119.
[31]杜国庆,丁道芳,李玲慧,等.骨关节炎软骨退变基因调控的研究进展.中国矫形外科杂志,2013,11:1089-1093.
[32]Kimura H,Yukitake H,Suzuki H,et al.The chondroprotective agent ITZ-1 inhibits interleukin-1beta-induced matrix metalloproteinase-13production and suppresses nitric oxide-induced chondrocyte death.J Pharmacol Sci,2009,2:201-211.
[33]Radons J,Bosserhoff AK,Grssel S,et al.p38MAPK mediates IL-1-induced down-regulation of aggrecan gene expression in human chondrocytes.Int J Mol Med,2006,4:661-668.
[34]Sondergaard BC,Schultz N,Madsen SH,et al.MAPKs are essential upstream signaling pathways in prote-olytic cartilage degradation-divergence in pathways leading to aggrecanase and MMP-mediated articular cartilage degradation.Osteoarthritis Cartilage,2010,3:279-288.
[35]Fahmi H,Martel-pelletier J,Pelletier JP,et al.Peroxisome proliferatoractivated receptor gamma in osteoarthritis.Mod Rheumatol,2011,1:1-9.