[1]杨轶,许治国,王亮.鼠尾草酚调节AMPK/NLRP3信号通路对H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应的影响[J].中国中医骨伤科杂志,2026,34(08):65-71.[doi:10.20085/j.cnki.issn1005-0205.260809]
 YANG Yi,XU Zhiguo,WANG Liang.The Effects of Carnosol on H2O2 -Induced Apoptosis,Oxidative Damage,and Inflammatory Response of Chondrocytes in Osteoarthritis by Regulating the AMPK/NLRP3 Signaling Pathway[J].Chinese Journal of Traditional Medical Traumatology & Orthopedics,2026,34(08):65-71.[doi:10.20085/j.cnki.issn1005-0205.260809]
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鼠尾草酚调节AMPK/NLRP3信号通路对H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应的影响()

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

卷:
第34卷
期数:
2026年08期
页码:
65-71
栏目:
基础研究
出版日期:
2026-08-10

文章信息/Info

Title:
The Effects of Carnosol on H2O2 -Induced Apoptosis,Oxidative Damage,and Inflammatory Response of Chondrocytes in Osteoarthritis by Regulating the AMPK/NLRP3 Signaling Pathway
文章编号:
1005-0205(2026)08-0065-07
作者:
杨轶1许治国1王亮1
1唐山市中医医院(河北 唐山,063099)
Author(s):
YANG Yi1XU Zhiguo1WANG Liang1
1Tangshan Hospital of Traditional Chinese Medicine,Tangshan 063099,Hebei China.
关键词:
鼠尾草酚 AMPK/NLRP3信号通路 骨关节炎 软骨细胞 凋亡 氧化损伤 炎症反应
Keywords:
carnosol AMPK/NLRP3 signaling pathway osteoarthritis chondrocytes apoptosis oxidative damage inflammatory response
分类号:
R-33
DOI:
10.20085/j.cnki.issn1005-0205.260809
文献标志码:
A
摘要:
目的:探究鼠尾草酚(CAR)对H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应的影响,分析是否与单磷酸腺苷活化蛋白激酶(AMPK)/Nod样受体蛋白3(NLRP3)通路有关。方法:培养并分离小鼠原代软骨细胞,分为对照组(CK组)、CAR组、H2O2组、低/中/高剂量CAR组(L/M/H-CAR组)、H-CAR+AMPK抑制剂Compound C组(H-CAR+Compound C组)、CK+Compound C组。软骨细胞增殖、凋亡、活性氧(ROS)荧光强度检测分别用Calcein-AM、Hoechst 33342染色、DCFH-DA荧光探针法; 超氧化物歧化酶(SOD)、丙二醛(MDA)和肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、IL-8检测用ELISA; 软骨特异性蛋白及AMPK/NLRP3通路相关蛋白检测用Western Blot法。结果:成功实现原代软骨细胞分离及培养。CAR组、CK+Compound C组较CK组细胞增殖率、SOD、Col2α1、p-AMPK/AMPK、细胞凋亡率、活性氧荧光强度、丙二醛、TNF-α、IL-6、IL-8、NLRP3差异无统计学意义(P>0.05); H2O2组较CK组细胞增殖率、SOD、Col2α1、p-AMPK/AMPK降低,细胞凋亡率、活性氧荧光强度、丙二醛、TNF-α、IL-6、IL-8、NLRP3升高,差异有统计学意义(P<0.05); L/M/H-CAR组较H2O2组上述指标呈反向改变; 与H2O2组相比,H-CAR组细胞增殖率、SOD、Col2α1、p-AMPK/AMPK从38.64%±4.12%、(28.16±3.02)U/mL、0.30±0.04、0.31±0.04相应升至91.34%±8.37%、(62.78±6.46)U/mL、1.07±0.12、0.79±0.08,细胞凋亡率、活性氧荧光强度、丙二醛、TNF-α、IL-6、IL-8、NLRP3从31.57%±3.35%、68.15±7.02、(4.78±0.49)nmol/mL、(51.69±0.54)pg/mL、(32.09±3.37)pg/mL、(67.38±0.69)pg/mL、1.28±0.14相应降至6.78%±0.71%、12.34±1.38、(2.11±0.25)nmol/mL、(22.03±0.26)pg/mL、(10.07±1.10)pg/mL、(34.70±0.38)pg/mL、0.51±0.06; H-CAR+Compound C组较H-CAR组细胞增殖率、SOD、Col2α1、p-AMPK/AMPK降低,细胞凋亡率、活性氧荧光强度、丙二醛、TNF-α、IL-6、IL-8、NLRP3升高,差异有统计学意义(P<0.05)。结论:鼠尾草酚可能通过调控AMPK/NLRP3通路,减轻H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应,保护软骨细胞。
Abstract:
Objective:To explore the effects of carnosol(CAR)on apoptosis,oxidative damage,and inflammatory response of chondrocytes induced by H2O2 in osteoarthritis(OA),and to analyze whether isthey are related to the adenosine monophosphate activated protein kinase(AMPK)/Nod like receptor protein 3(NLRP3)pathway.Methods:Mouse primary chondrocytes were culturedisolated and isolated,cultured,and assigned into control group(CK group),CAR group,H2O2 group,low,medium,and high-dose CAR groups(L,M,H-CAR groups),and H-CAR+AMPK inhibitor Compound C group(H-CAR+Compound C group),CK+Compound C group.The proliferation,apoptosis of chondrocytes,and ROS fluorescence intensity were detected using Calcein-AM,Hoechst 33342 staining,and DCFH-DA fluorescence probe method,respectively.The levels of SOD,MDA,TNF-α,IL-6,and IL-8 were measured using ELISA.In addition,Western Blot was used to measure cartilage specific proteins and AMPK/NLRP3 pathway related proteins.Results:The isolation and culture of primary chondrocytes were successfully achieved.There were no significant differences in cell proliferation rate,SOD,Col2α1 expression,p-AMPK/AMPK,cell apoptosis rate,ROS fluorescence intensity,MDA,TNF-α,IL-6,IL-8 levels,and NLRP3 expression between the CAR group,CK+Compound C group and the CK group(P>0.05).The H2O2 group showed decreased cell proliferation rate,SOD level,Col2α1 expression,and p-AMPK/AMPK,while increased apoptosis rate,ROS fluorescence intensity,MDA,TNF-α,IL-6,IL-8 levels,and NLRP3 protein expression than the CK group(P<0.05).Compared with the H2O2 group,the aforementioned indicators in the L-,M-,and H-CAR groups exhibited opposite changes.Compared with the H2O2 group,the cell proliferation rate,SOD,Col2α1 expression,and p-AMPK/AMPK in the H-CAR group increased from 38.64%±4.12%,(28.16±3.02)U/mL,0.30±0.04,and 0.31±0.04 to 91.34%±8.37%,(62.78±6.46)U/mL,1.07±0.12,and 0.79±0.08,respectively; the cell apoptosis rate,ROS fluorescence intensity,levels of MDA,TNF-α,IL-6,and IL-8,and NLRP3 expression decreased from 31.57%±3.35%,68.15±7.02,(4.78±0.49)nmol/mL,(51.69±0.54)pg/mL,(32.09±3.37)pg/mL,(67.38±0.69)pg/mL,and 1.28±0.14 to 6.78%±0.71%,12.34±1.38,(2.11±0.25)nmol/mL,(22.03±0.26)pg/mL,(10.07±1.10)pg/mL,(34.70±0.38)pg/mL,and 0.51±0.06,respectively.The H-CAR+Compound C group showed decreased cell proliferation rate,SOD,Col2α1 expression,and p-AMPK/AMPK,while increased apoptosis rate,ROS fluorescence intensity,MDA,TNF-α,IL-6,IL-8 levels,and NLRP3 expression than the H-CAR group(P<0.05).Conclusion:CAR may alleviate H2O2 induced apoptosis,oxidative damage,and inflammatory response in OA chondrocytes by regulating the AMPK/NLRP3 pathway,thereby exerting a protective effect on chondrocytes.

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(收稿日期:2025-10-29)

备注/Memo

备注/Memo:
基金项目:河北省中医药管理局科研计划项目(2024425)
更新日期/Last Update: 2026-08-15