[2] Yoshimura N,Muraki S,Oka H,et al. Cohort profile:research on Osteoarthritis/Osteoporosis Against Disability study[J]. Int J Epidemiol, 2010,39(4):988-995.
[3] Azzini GOM, Santos GS, Visoni SBC, et al. Metabolic syndrome and subchondral bone alterations: The rise of osteoarthritis - A review[J]. J Clin Orthop Trauma, 2020, 11(Suppl 5):S849-S855.
[4] Kraus VB,Yan Z. Induction of osteoarthritis and metabolic inflammation by a very high fat diet in mice:effects of short term exercise[J]. Arthritis Rheum, 2012, 64(2):443-453.
[5] Ioanna P, Konstantinos NM, Aspasia T. Bone morphogenetic protein-2-induced Wnt/bcatenin signaling pathway activation through enhanced low-density-lipoprotein receptorrelated protein 5 catabolic activity contributes to hypertrophy in osteoarthritic chondrocytes[J].Arthritis Res,2012,14(2):1-14.
[6] Pelletieer JP,Faure MP,Dibattisa JA,et al.Coovd inatesgnthes is of stromglisine interleukin-1 and oncogeneproteins in experimental osteoarthritis,Animmunohi Stochemical study[J].Am J Pathol,2010,142:95-105.
[7] Hangtian Wu,Ting Xu,Zhigang Chen,et al.Goldring SR. Specific inhibition of FAK signaling attenuates subchondral bone deterioration and articular cartilage degeneration during osteoarthritis pathogenesis[J].J Cell Physiol, 2020, 235(11):8653-8666.
[8] Zahan OM, Serban O, Gherman C, et al. The evaluation of oxidative stress in osteoarthritis[J].Med Pharm Rep, 2020, 93(1):12-22.
[9] Wang F,Ying Z,Duan X,et al. Histomorphometric analysis of adult articular calcified cartilage zone[J].J Struct Biol, 2009,168 (3):359-365.
[10] Fosang AJ,Last K,Maciewlcz RA. Aggrecan is degraded hy matrix Metall-oprotenases in human arthritis,Evidence that matrix Metallproteinase and aggrecanases activites can be independent[J].Clin Invent, 2011, 98:2292.
[11] Wang,M. Recent progress in understanding molecular mechanisms ofcartilage degeneration during osteoarthritis[J].Ann N Y Acad Sci, 2011, 1240: 61-69.
[12] Cui N, Hu M, Khalil RA. Biochemical and Biological Attributes of Matrix Metalloproteinases[J].Prog Mol Biol Transl Sci, 2017,147:1-73
[13] VilmontV,L.Toumeur, G Chiocchia. Fas-associated death domain protein and adenosine partnership: fad in RA[J].Rheumatology (Oxford), 2012,51(6): 964-975.
[14] Arpino V, Brock M, Gill SE. The role of TIMPs in regulation of extracellular matrix proteolysis[J].Matrix Biol,2015,44:247-254.
[15] Gilbert, S.J. Protein kinase R plays a pivotal role in oncostatin M and interlexikin-l signalling in bovine articular cartilage chondrocytes[J].Eur Cell Mater, 2012, 23: 41-57.
[16] Medeiros,A. Prostaglandin E2 and the suppression of phagocyte innate immune responses in different organs[J].Mediators Inflamm,2012, 2012(5):327568.
[17] Han Ol Kwon,Minhee Lee,Ok-Kyung Kim,et al. Effect of Hijikia fusiforme extracts on degenerative osteoarthritis in vitro and in vivo models[J].Nutr Res Pract,2016,10(3):265-273.
[18] G Ozen,S Boumiza,C Deschildre, et al. Inflammation increases MMP levels via PGE 2 in human vascular wall and plasma of obese women[J].Int J Obes (Lond),2019,43(9):1724-1734.
[19] Huh,J.E. WIN-34B,a new herbal medicine,inhibits the inflammatory response by inactivating HcappaB-alpha phosphorylation and mitogen activated protein kinase pathways in fibroblast-like synoviocytes[J].J Ethnopharmacol, 2012,143(3): 779-786.
[20] Bin He,Fei Wu,Xiaohai Li,et al. Mitochondrial dependent pathway is involved in the protective effects of carboxymethylated chitosan on nitric oxide-induced apoptosis in chondrocytes[J].BMC Complement Med Ther, 2020,20(1):23.","bibtexUrl_cn":"//www.pitakata.com/xuebao/CN/article/getTxtFile.do?fileType=BibTeX&id=2","abstractUrl_en":"http://xuebao.sdfmu.edu.cn/EN/10.3969/j.issn.2097-0005.2021.06.002","qi":"6","id":2,"nian":2021,"bianHao":"1629870988168-1294137388","zuoZheEn_L":"Hou Shenggui, Liu Jianqiang","juanUrl_en":"http://xuebao.sdfmu.edu.cn/EN/Y2021","clcIndexList_en":[{"code":"R684","text":""}],"shouCiFaBuRiQi":"2021-08-25","qiShiYe":"406","received":"2020-12-13","qiUrl_cn":"http://xuebao.sdfmu.edu.cn/CN/Y2021/V42/I6","lanMu_cn":"基础研究","pdfSize":"3809","zuoZhe_CN":"侯圣贵, 刘建强","risUrl_cn":"//www.pitakata.com/xuebao/CN/article/getTxtFile.do?fileType=Ris&id=2","title_cn":"乙酰水杨酸联合双氯芬酸治疗骨关节炎的机制","doi":"10.3969/j.issn.2097-0005.2021.06.002","jieShuYe":"410","keywordList_en":["acetylsalicylic acid combined with diclofenac","osteoarthritis","MMPs","TIMP"],"endNoteUrl_cn":"//www.pitakata.com/xuebao/CN/article/getTxtFile.do?fileType=EndNote&id=2","zhaiyao_en":"Objective: To study the mechanism of combination diclofenac with different concentrations of acetylsalicylic acid in rabbit osteoarthritis models. Methods: Rabbit osteoarthritis models were treated with diclofenac acetyl in accordance with different concentrations of alicylic acid. We measured the scores in articular cartilage.PCR and WB were performed to detect the expressions of MMP-3 and TIMP-1.ELASA was used to compare the NO and IL-1β in synovial fluid. Results: Different concentrations of the drug had good therapeutic effect on osteoarthritis of rabbit knee,reduced the scores and the contents of NO and IL-1β,WB method showed the expressions of MMP-3 and MMP-13 protein were down regulated,PCR found upregulation mRNA expression of TIMP-1. Conclusion: Combination of diclofenac with different concentrations of acetylsalicylic acid can relieve the pathological changes in our rabbit osteoarthritis models.The effective therapeutic regimen for osteoarthritis can be verified.The therapeutic goal for osteoarthritis models is achieved by the inhibition of NO, IL-1,MMP-3 and MMP-13 expression, accompanied by the uprugulation of TIMP-1 expression.","bibtexUrl_en":"http://xuebao.sdfmu.edu.cn/EN/article/getTxtFile.do?fileType=BibTeX&id=2","abstractUrl_cn":"http://xuebao.sdfmu.edu.cn/CN/10.3969/j.issn.2097-0005.2021.06.002","zuoZheCn_L":"侯圣贵, 刘建强","juanUrl_cn":"http://xuebao.sdfmu.edu.cn/CN/Y2021","lanMu_en":"Basic Researches","clcIndexList_cn":[{"code":"R684","text":""}],"qiUrl_en":"//www.pitakata.com/xuebao/EN/Y2021/V42/I6","zuoZhe_EN":"Hou Shenggui, Liu Jianqiang","risUrl_en":"http://xuebao.sdfmu.edu.cn/EN/article/getTxtFile.do?fileType=Ris&id=2","title_en":"Mechanism of acetylsalicylic acid combined with diclofenac in the treatment of osteoarthritis","hasPdf":"true"},"authorNotes_cn":["候圣贵(1966—),副主任药师,本科,主要从事临床药学工作。E-mail:hsgjinan@163.com。"],"authorList_en":[{"deceased":false,"name_cn":"侯圣贵","name_en":"Hou Shenggui"},{"deceased":false,"name_cn":" 刘建强","name_en":" Liu Jianqiang"}]}">

Mechanism of acetylsalicylic acid combined with diclofenac in the treatment of osteoarthritis

Hou Shenggui, Liu Jianqiang

Journal of ShanDong First Medical University&ShanDong Academy of Medical Sciences››2021, Vol. 42››Issue (6): 406-410.

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PDF(3809 KB)
Journal of ShanDong First Medical University&ShanDong Academy of Medical Sciences ›› 2021, Vol. 42 ›› Issue (6) : 406-410. DOI: 10.3969/j.issn.2097-0005.2021.06.002
Basic Researches

Mechanism of acetylsalicylic acid combined with diclofenac in the treatment of osteoarthritis

  • Hou Shenggui, Liu Jianqiang
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Abstract

Objective: To study the mechanism of combination diclofenac with different concentrations of acetylsalicylic acid in rabbit osteoarthritis models. Methods: Rabbit osteoarthritis models were treated with diclofenac acetyl in accordance with different concentrations of alicylic acid. We measured the scores in articular cartilage.PCR and WB were performed to detect the expressions of MMP-3 and TIMP-1.ELASA was used to compare the NO and IL-1β in synovial fluid. Results: Different concentrations of the drug had good therapeutic effect on osteoarthritis of rabbit knee,reduced the scores and the contents of NO and IL-1β,WB method showed the expressions of MMP-3 and MMP-13 protein were down regulated,PCR found upregulation mRNA expression of TIMP-1. Conclusion: Combination of diclofenac with different concentrations of acetylsalicylic acid can relieve the pathological changes in our rabbit osteoarthritis models.The effective therapeutic regimen for osteoarthritis can be verified.The therapeutic goal for osteoarthritis models is achieved by the inhibition of NO, IL-1,MMP-3 and MMP-13 expression, accompanied by the uprugulation of TIMP-1 expression.

Key words

acetylsalicylic acid combined with diclofenac/osteoarthritis/MMPs/TIMP

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Hou Shenggui, Liu Jianqiang.Mechanism of acetylsalicylic acid combined with diclofenac in the treatment of osteoarthritis[J]. Journal of ShanDong First Medical University&ShanDong Academy of Medical Sciences. 2021, 42(6): 406-410 https://doi.org/10.3969/j.issn.2097-0005.2021.06.002

References

[1] Barrouin-Melo SM, Anturaniemi J, Sankari S, et al. Evaluating oxidative stress, serological- and haematological status of dogs suffering from osteoarthritis, after supplementing their diet with fish or corn oil[J]. Lipids Health Dis, 2016,15(1):139.
[2] Yoshimura N,Muraki S,Oka H,et al. Cohort profile:research on Osteoarthritis/Osteoporosis Against Disability study[J]. Int J Epidemiol, 2010,39(4):988-995.
[3] Azzini GOM, Santos GS, Visoni SBC, et al. Metabolic syndrome and subchondral bone alterations: The rise of osteoarthritis - A review[J]. J Clin Orthop Trauma, 2020, 11(Suppl 5):S849-S855.
[4] Kraus VB,Yan Z. Induction of osteoarthritis and metabolic inflammation by a very high fat diet in mice:effects of short term exercise[J]. Arthritis Rheum, 2012, 64(2):443-453.
[5] Ioanna P, Konstantinos NM, Aspasia T. Bone morphogenetic protein-2-induced Wnt/bcatenin signaling pathway activation through enhanced low-density-lipoprotein receptorrelated protein 5 catabolic activity contributes to hypertrophy in osteoarthritic chondrocytes[J].Arthritis Res,2012,14(2):1-14.
[6] Pelletieer JP,Faure MP,Dibattisa JA,et al.Coovd inatesgnthes is of stromglisine interleukin-1 and oncogeneproteins in experimental osteoarthritis,Animmunohi Stochemical study[J].Am J Pathol,2010,142:95-105.
[7] Hangtian Wu,Ting Xu,Zhigang Chen,et al.Goldring SR. Specific inhibition of FAK signaling attenuates subchondral bone deterioration and articular cartilage degeneration during osteoarthritis pathogenesis[J].J Cell Physiol, 2020, 235(11):8653-8666.
[8] Zahan OM, Serban O, Gherman C, et al. The evaluation of oxidative stress in osteoarthritis[J].Med Pharm Rep, 2020, 93(1):12-22.
[9] Wang F,Ying Z,Duan X,et al. Histomorphometric analysis of adult articular calcified cartilage zone[J].J Struct Biol, 2009,168 (3):359-365.
[10] Fosang AJ,Last K,Maciewlcz RA. Aggrecan is degraded hy matrix Metall-oprotenases in human arthritis,Evidence that matrix Metallproteinase and aggrecanases activites can be independent[J].Clin Invent, 2011, 98:2292.
[11] Wang,M. Recent progress in understanding molecular mechanisms ofcartilage degeneration during osteoarthritis[J].Ann N Y Acad Sci, 2011, 1240: 61-69.
[12] Cui N, Hu M, Khalil RA. Biochemical and Biological Attributes of Matrix Metalloproteinases[J].Prog Mol Biol Transl Sci, 2017,147:1-73
[13] VilmontV,L.Toumeur, G Chiocchia. Fas-associated death domain protein and adenosine partnership: fad in RA[J].Rheumatology (Oxford), 2012,51(6): 964-975.
[14] Arpino V, Brock M, Gill SE. The role of TIMPs in regulation of extracellular matrix proteolysis[J].Matrix Biol,2015,44:247-254.
[15] Gilbert, S.J. Protein kinase R plays a pivotal role in oncostatin M and interlexikin-l signalling in bovine articular cartilage chondrocytes[J].Eur Cell Mater, 2012, 23: 41-57.
[16] Medeiros,A. Prostaglandin E2 and the suppression of phagocyte innate immune responses in different organs[J].Mediators Inflamm,2012, 2012(5):327568.
[17] Han Ol Kwon,Minhee Lee,Ok-Kyung Kim,et al. Effect of Hijikia fusiforme extracts on degenerative osteoarthritis in vitro and in vivo models[J].Nutr Res Pract,2016,10(3):265-273.
[18] G Ozen,S Boumiza,C Deschildre, et al. Inflammation increases MMP levels via PGE 2 in human vascular wall and plasma of obese women[J].Int J Obes (Lond),2019,43(9):1724-1734.
[19] Huh,J.E. WIN-34B,a new herbal medicine,inhibits the inflammatory response by inactivating HcappaB-alpha phosphorylation and mitogen activated protein kinase pathways in fibroblast-like synoviocytes[J].J Ethnopharmacol, 2012,143(3): 779-786.
[20] Bin He,Fei Wu,Xiaohai Li,et al. Mitochondrial dependent pathway is involved in the protective effects of carboxymethylated chitosan on nitric oxide-induced apoptosis in chondrocytes[J].BMC Complement Med Ther, 2020,20(1):23.
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