[1]白龙,赵泽恪,王明源,等.羟基红花黄色素A对白细胞介素-1β诱导的髓核细胞凋亡和炎症反应的影响机制探讨[J].中国中医骨伤科杂志,2025,33(10):8-14.[doi:10.20085/j.cnki.issn1005-0205.251002]
　BAI Long,ZHAO Zeke,WANG Mingyuan,et al.The Mechanism Explore for Hydroxysafflor Yellow A on Apoptosis and Inflammatory Response of Nucleus Pulposus Cells Induced by Interleukin-1β[J].Chinese Journal of Traditional Medical Traumatology & Orthopedics,2025,33(10):8-14.[doi:10.20085/j.cnki.issn1005-0205.251002]
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羟基红花黄色素A对白细胞介素-1β诱导的髓核细胞凋亡和炎症反应的影响机制探讨()

《中国中医骨伤科杂志》[ISSN:1005-0205/CN:42-1340/R]

卷:
第33卷
期数:
2025年10期
页码:
8-14
栏目:
实验研究
出版日期:
2025-10-15

文章信息/Info

Title:
The Mechanism Explore for Hydroxysafflor Yellow A on Apoptosis and Inflammatory Response of Nucleus Pulposus Cells Induced by Interleukin-1β
文章编号:
1005-0205(2025)10-0008-07
作者:
白龙1; 赵泽恪1; 王明源1; 温静2△
1太原市中医医院(太原,030009)
2晋中市第一人民医院
Author(s):
BAI Long1; ZHAO Zeke1; WANG Mingyuan1; WEN Jing2△
1Taiyuan Traditional Chinese Medicine Hospital,Taiyuan 030009,China; 2Jinzhong First People's Hospital,Jinzhong 030600,Shanxi China.
关键词:
羟基红花黄色素A;  核转录因子-κB/NOD样受体蛋白3信号通路;  白细胞介素-1β;  髓核细胞;  凋亡;  炎症反应
Keywords:
hydroxysafflor yellow A;  NF-κB/NLRP3 signaling pathway;  IL-1β;  nucleus pulposus cells;  apoptosis;  inflammatory response
分类号:
R285.5
DOI:
10.20085/j.cnki.issn1005-0205.251002
文献标志码:
A
摘要:
目的:探讨羟基红花黄色素A(HSYA)对白细胞介素-1β(IL-1β)诱导的髓核细胞(NPC)凋亡和炎症反应及核转录因子-κB(NF-κB)/NOD样受体蛋白3(NLRP3)信号通路的影响。方法:将髓核细胞随机分为正常(CK)组、髓核细胞(Model)组(10 ng/mL IL-1β处理)、低剂量羟基红花黄色素A(L-HSYA)组(10 ng/mL IL-1β+25 μmol/L HSYA)、中剂量羟基红花黄色素A(M-HSYA)组(10 ng/mL IL-1β+50 μmol/L HSYA)、高剂量羟基红花黄色素A(H-HSYA)组(10 ng/mL IL-1β+100 μmol/L HSYA)、H-HSYA+NF-κB激活剂脂多糖(LPS)(H-HSYA+LPS)组(10 ng/mL IL-1β+100 μmol/L HSYA+4.0 μg/mL LPS)。流式细胞术、Hochest 33258染色检测细胞凋亡,CCK-8法、ELISA法及Western Blot分别检测细胞活性、TNF-α、IL-6、IL-8、NO水平以及COX-2、iNOS、Bax、Bcl-2、Caspase-3、p-NF-κB p65、NF-κB p65、NLRP3蛋白表达。结果:与正常组比较,髓核细胞组细胞光密度(OD)值、Bcl-2蛋白表达降低,凋亡率、TNF-α、IL-6、IL-8、NO水平、COX-2、iNOS、Bax、Caspase-3、p-NF-κB p65/NF-κB p65、NLRP3蛋白表达升高(P<0.05); 与髓核细胞组比较,L-HSYA组、M-HSYA组、H-HSYA组OD值、Bcl-2蛋白表达升高,凋亡率、TNF-α、IL-6、IL-8、NO水平、COX-2、iNOS、Bax、Caspase-3、p-NF-κB p65/NF-κB p65、NLRP3蛋白表达降低(P<0.05); 与H-HSYA组比较,H-HSYA+LPS组OD值、Bcl-2蛋白表达降低,凋亡率、TNF-α、IL-6、IL-8、NO水平、COX-2、iNOS、Bax、Caspase-3、p-NF-κB p65/NF-κB p65、NLRP3蛋白表达升高(P<0.05)。结论:羟基红花黄色素A可能通过抑制NF-κB/NLRP3信号通路进而减轻IL-1β诱导的髓核细胞凋亡和炎症反应。
Abstract:
Objective:To investigate the effects of hydroxysafflor yellow A(HSYA)on interleukin-1β(IL-1β)-induced apoptosis and inflammatory response of nucleus pulposus cells(NPCs),as well as the nuclear factor-κB(NF-κB)/NOD-like receptor protein 3(NLRP3)signaling pathway.Methods:NPCs stochastically divided into normal(CK)group,NPC(Model)group(treated with 10 ng/mL IL-1β),low-dose HSYA(L-HSYA)group(10 ng/mL IL-1β+25 μmol/L HSYA),medium dose HSYA(M-HSYA)group(10 ng/mL IL-1β+50 μmol/L HSYA),high-dose HSYA(H-HSYA)group(10 ng/mL IL-1β+100 μmol/L HSYA),and H-HSYA+NF-κB activator Lipopolysaccharide(LPS)(H-HSYA+LPS)group(10 ng/mL IL-1β+100 μmol/L HSYA+4.0 μg/mL LPS).Detect cell apoptosis by flow cytometry and Hoechst 33258 staining.CCK-8 method,ELISA method,and Western Blot were performed to detect cell viability,TNF-α,IL-6,IL-8,NO levels,and COX-2,iNOS,Bax,Bcl-2,Caspase-3,p-NF-κB p65,NF-κB p65,and NLRP3 protein expression.Results:Compared with CK group,the OD value and Bcl-2 protein expression were lower in Model group,while the apoptosis rate,TNF-α,IL-6,IL-8,NO levels,COX-2,iNOS,Bax,Caspase-3,p-NF-κB p65/NF-κB p65,and NLRP3 protein expression were higher(P<0.05).Compared with Model group,the OD value and Bcl-2 protein expression were higher in L-HSYA,M-HSYA,and H-HSYA groups,while the apoptosis rate,TNF-α,IL-6,IL-8,NO levels,COX-2,iNOS,Bax,Caspase-3,p-NF-κB p65/NF-κB p65,and NLRP3 protein expression were lower(P<0.05).Compared with H-HSYA group,the OD value and Bcl-2 protein expression were lower in H-HSYA+LPS group,while the apoptosis rate,TNF-α,IL-6,IL-8,NO levels,COX-2,iNOS,Bax,Caspase-3,p-NF-κB p65/NF-κB p65,and NLRP3 protein expression were higher(P<0.05).Conclusion:HSYA may alleviate IL-1β-induced NPC apoptosis and inflammatory response by inhibiting NF-κB/NLRP3 signaling pathway.

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(收稿日期:2025-03-19)

备注/Memo

备注/Memo:
△通信作者 E-mail:13753149630@163.com
更新日期/Last Update: 2025-10-10