[1]梁小弟,梁小菊,李芙蓉,等.Smad核相互作用蛋白1在白细胞介素-1β诱导骨关节炎中的作用及机制实验研究[J].陕西医学杂志,2021,50(4):390-394.[doi:DOI:10.3969/j.issn.1000-7377.2021.04.002]
 LIANG Xiaodi,LIANG Xiaoju,LI Furong,et al.Role and mechanism of SNIP1 in IL-1β-induced osteoarthritis[J].,2021,50(4):390-394.[doi:DOI:10.3969/j.issn.1000-7377.2021.04.002]
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Smad核相互作用蛋白1在白细胞介素-1β诱导骨关节炎中的作用及机制实验研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
50
期数:
2021年4期
页码:
390-394
栏目:
基础研究
出版日期:
2021-04-05

文章信息/Info

Title:
Role and mechanism of SNIP1 in IL-1β-induced osteoarthritis
作者:
梁小弟1梁小菊2李芙蓉3石茂才1
(1.定西市人民医院骨二科,甘肃 定西 743000; 2.西安交通大学附属红会医院小儿骨科,陕西 西安 710054; 3.定西市人民医院麻醉科,甘肃 定西 743000)
Author(s):
LIANG XiaodiLIANG XiaojuLI FurongSHI Maocai
(Department of Orthopedics,Dingxi People's Hospital,Dingxi 743000,China)
关键词:
Smad核相互作用蛋白1 骨关节炎 软骨细胞 NF-κB信号通路 炎症
Keywords:
Smad nuclear interaction protein 1 Osteoarthritis Chondrocyte NF-κB signaling pathway Inflammation
分类号:
R 684.3
DOI:
DOI:10.3969/j.issn.1000-7377.2021.04.002
文献标志码:
A
摘要:
目的:探究Smad核相互作用蛋白1(SNIP1)在白细胞介素-1β(IL-1β)诱导骨关节炎中的作用及机制。方法:不同浓度IL-1β处理NHAC-κn细胞24 h后,用CCK-8检测细胞活性。逆转录聚合酶链式反应(RT-PCR)和免疫印迹分析法检测SNIP1在骨关节炎细胞模型中的表达。ELISA和免疫印迹分析法检测炎症相关蛋白表达及NF-κB信号通路蛋白磷酸化细胞核因子-κBp65(p-p65)、磷酸化细胞核因子抑制蛋白(p-IκB)的磷酸化。结果:与未经IL-1β处理的NHAC-κn相比,IL-1β抑制细胞活性并下调SNIP1的mRNA和蛋白表达水平。在IL-1β处理的NHAC-κn中,SNIP1过表达载体(pcDNA3.1-SNIP1)显著抑制一氧化氮合酶(iNOS)、环氧合酶-2(COX-2)、抗基质金属蛋白酶-3(MMP-3)、MMP-13、ADAMTS-5的表达,促进抗Ⅱ型胶原(Collagen Ⅱ)、抗聚集蛋白聚糖(Aggrecan)合成。Betulinic acid(NF-κB激活剂)可逆转pcDNA3.1-SNIP1对p-p65、p-IκB及炎症因子(IL-6、TNF-α)的抑制作用。结论:SNIP1过表达可能通过抑制NF-κB信号通路的活性来缓解软骨细胞炎症反应,SNIP1有望成为治疗骨关节炎的潜在靶点。
Abstract:
bjective:To investigate the role and mechanism of Smad nuclear interaction protein 1(SNIP1)in IL-1β-induced osteoarthritis.Methods:After treating NHAC-κn cells with different concentrations of IL-1β for 24 hours,CCK-8 was used to detect the cell activity.Expression of SNIP1 in osteoarthritis cell model was detected by RT-PCR and Western blot.ELISA and Western blot analysis were recruited to detect the expression of inflammation-related proteins and phosphorylation of NF-κB signaling proteins p65 and p-IκB.Results:Compared with IL-1β-untreated NHAC-κn,IL-1β inhibited cell activity and down-regulated SNIP1 mRNA and protein expression levels.pcDNA3.1-SNIP1 significantly inhibited the expression of iNOS,COX-2,MMP-3,MMP-13,and ADAMTS-5 in NHAC-κn treated with IL-1β,and promoted Collagen Ⅱ and Aggrecan synthesis.Betulinic acid(NF-κB activator)reversed the inhibitory effect of pcDNA3.1-SNIP1 on the levels of p-p65,p-IκB and inflammatory factors(IL-6,TNF-α).Conclusion:The overexpression of SNIP1 may alleviate the inflammatory response of chondrocytes by inhibiting the activity of NF-κB signaling pathway,and SNIP1 is expected to be a potential target for the treatment of osteoarthritis.

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备注/Memo

备注/Memo:
基金项目:甘肃省定西市科技计划项目(DX2020Z01-4)
更新日期/Last Update: 2021-04-06