双醋瑞因介导软骨细胞焦亡修复骨关节炎软骨损伤的机制研究

doi:10.3969/j.issn.1006-6233.2022.12.004

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Abstract Objective: To explore the mechanism of diacetylruiyin affecting cartilage injury in osteoarthritis. Methods: Cartilage cell lines were purchased for induction of osteoarthritic cartilage injury model by LPS, and the expression levels of miR-107 and SMAD2 were detected by qRT-PCR. Western blot was used to detect the expression level of SMAD2 and pyroptosis related protein Caspase-1; ELISA was used to detect the expression of inflammatory cytokines IL-1β and IL-18; starbase database and the dual luciferase assay was used to predict and verify the target binding sites of miR-107 and SMAD2. Results: Compared with the Blank group, the miR-107 level in the LPS group was obviously decreased, and the SMAD2 level was significantly increased. At the same time, LPS decreased the Caspase-1 level, and increased the expressions of inflammatory factors IL-1β and IL-18 dramatically. However, transfecting miR-107 mimic partially reversed results which LPS-induced. After the cell model was treated with diacerein, the level of miR-107 and Caspase-1 protein were increased, the level of SMAD2 and inflammatory factors were significantly decreased. Conclusion: Diacetin can repair osteoarthritis cartilage injury by miR-107/SMAD2.

Key words： Osteoarthritis Cartilage injury Diacerein Cartilage cell pyroptosis

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	YUAN Lei
	LIU Zhiyuan
	XUE Tao
	et al

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YUAN Lei,LIU Zhiyuan,XUE Tao, et al. Study on the Mechanism of Cartilaginous Cell Pyroptosis Mediated by Diacerein in Repairing Cartilage Injury in Osteoarthritis[J]. HeBei Med, 2022, 28(12): 1956-1960.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.12.004 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I12/1956

[1] Neogi T.The epidemiology and impact of pain in osteoarthritis[J].Osteoarthritis Cartilage,2013,21(9):1145-1153.
[2] Kloppenburg M,F Berenbaum.Osteoarthritis year in review 2019:epidemiology and therapy[J].Osteoarthritis Cartilage,2020,28(3):242-248.
[3] Ashkavand Z,H Malekinejad,B S Vishwanath.The pathophysiology of osteoarthritis[J].Journal of Pharmacy Research,2013,7(1):132-138.
[4] Moskowitz R W.The burden of osteoarthritis:clinical and quality-of-life issues[J].The American Journal of Managed Care,2009,15(8 Suppl):223-229.
[5] Panova E,G Jones.Benefit-risk assessment of diacerein in the treatment of osteoarthritis[J].Drug Safety,2015,38(3):245-252.
[6] Gargano G,et al.Small interfering RNAs in tendon homeostasis[J].British Medical Bulletin,2021,138(1):58-67.
[7] Oliviero A,et al.MicroRNA in osteoarthritis:physiopathology,diagnosis and therapeutic challenge[J].British Medical Bulletin,2019,130(1):137-147.
[8] Li G-S,L Cui,G-D Wang.miR-155-5p regulates macrophage M1 polarization and apoptosis in the synovial fluid of patients with knee osteoarthritis[J].Exp Ther Med,2021,21(1):68.
[9] Zhou B,et al.Tanshinone ⅡA ameliorates inflammation response in osteoarthritis via inhibition of miR-155/FOXO3 axis[J].Pharmacology,2021,106(1-2):20-28.
[10] Shi J,et al.miR-486-5p is upregulated in osteoarthritis and inhibits chondrocyte proliferation and migration by suppressing SMAD2[J].Mol Med Rep,2018,18(1):502-508.
[11] Fu Q,et al.NLRP3/caspase-1 pathway-induced pyroptosis mediated cognitive deficits in a mouse model of sepsis-associated encephalopathy[J].Inflammation,2019,42(1):306-318.
[12] Rajamki K,et al.Cholesterol crystals activate the NLRP3 inflammasome in human macrophages:a novel link between cholesterol metabolism and inflammation[J].PloS one,2010,5(7):11765.
[24] Akahoshi T,Y Murakami,H Kitasato.Recent advances in crystal-induced acute inflammation[J].Current opinion in rheumatology,2007,19(2):146-150.
[25] Kolly L,et al.Inflammatory role of ASC in antigen-induced arthritis is independent of caspase-1,NALP-3,and IPAF[J].The Journal of Immunology,2009,183(6):4003-4012.
[26] Zhang Y,Y Zheng,H Li.NLRP3 inflammasome plays an important role in the pathogenesis of collagen-induced arthritis[J].Mediators of Inflammation,2016,2016.
[27] Denoble A E,et al.Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation[J].Proceedings of the National Academy of Sciences,2011,108(5):2088-2093.
[28] Qi H,L Yao.Advances in the mechanism of pyroptosis activation and related diseases[J].Journal of Chinese Practical Diagnosis and Therapy,2016,30(5):417-419.
[29] Liu W,Z Zha,H Wang.Upregulation of microRNA-27a inhibits synovial angiogenesis and chondrocyte apoptosis in knee osteoarthritis rats through the inhibition of PLK2[J].Journal of Cellular Physiology,2019,234(12):22972-22984.
[30] Gu R,et al.MicroRNA-9 regulates the development of knee osteoarthritis through the NF-kappaB1 pathway in chondrocytes[J].Medicine,2016,95(36).
[31] Tian F,et al.miR-107 modulates chondrocyte proliferation,apoptosis,and extracellular matrix synthesis by targeting PTEN[J].International Journal of Clinical and Experimental Pathology,2019,12(2):488.
[32] Lin S-S,et al.Hyperbaric oxygen inhibits the HMGB1/RAGE signaling pathway by upregulating Mir-107 expression in human osteoarthritic chondrocytes[J].Osteoarthritis and cartilage,2019,27(9):1372-1381.