电针通过调控TLR4/MyD88/NF-κB信号通路减轻膝关节骨关节炎大鼠膝关节软骨凋亡

doi:10.12122/j.issn.1673-4254.2026.08.16

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (8): 1886-1895.doi: 10.12122/j.issn.1673-4254.2026.08.16

• • 上一篇

电针通过调控TLR4/MyD88/NF-κB信号通路减轻膝关节骨关节炎大鼠膝关节软骨凋亡

李春宁¹(), 杨琪琪², 张振丰¹, 鲍亮¹, 姜天鑫², 张玉³, 李飞²()

^1.安徽中医药大学第二临床医学院，安徽合肥 230061
^2.安徽中医药大学第二附属医院康复二科，安徽合肥 230061
^3.阜阳市中医医院针灸科，安徽阜阳 236001

收稿日期:2025-12-04 出版日期:2026-08-20 发布日期:2026-08-01
通讯作者: 李飞 E-mail:1141693303@qq.com;leagcen@163.com
作者简介:李春宁，在读硕士研究生，E-mail: 1141693303@qq.com
基金资助:
国家青年岐黄学者支持项目(国中医药人教函（2022）256号);第九批安徽省特支计划人才项目(皖组办字〔2023〕35号);安徽省华佗中医药研究院科技重大专项(BZKZ2401);安徽省自然科学基金面上项目(2308085MH297);安徽高校自然科学重大研究项目(2023AH040099);安徽省临床医学研究转化专项(202427b10020060);安徽省高等学校科学研究重点项目(2024AH050918);阜阳市重点研究与开发计划项目(FK20245541);安徽中医药大学“基础-临床融合”专项(JCLCA2025007)

Electroacupuncture alleviates articular chondrocyte apoptosis in rats with knee osteoarthritis by regulating the TLR4/MyD88/NF-κB signaling pathway

Chunning LI¹(), Qiqi YANG², Zhenfeng ZHANG¹, Liang BAO¹, Tianxin JIANG², Yu ZHANG³, Fei LI²()

^1.Second Clinical Medical College of Anhui University of Chinese Medicine, Hefei 230061, China
^2.Second Department of Rehabilitation, Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230061, China
^3.Department of Acupuncture, Fuyang Traditional Chinese Medicine Hospital, Fuyang 236001, China

Received:2025-12-04 Online:2026-08-20 Published:2026-08-01
Contact: Fei LI E-mail:1141693303@qq.com;leagcen@163.com

摘要/Abstract

摘要：

目的探讨电针调控Toll样受体4（TLR4）/髓样分化因子88（MyD88）/核转录因子-κB（NF-κB）信号通路对膝关节骨关节炎（KOA）大鼠软骨组织凋亡的影响。方法 27只SPF级SD大鼠随机分为空白组、模型组和电针组（n=9）。采用碘乙酸钠（MIA）法复制KOA大鼠模型。电针组予“内膝眼”“犊鼻”“血海”“阳陵泉”电针干预（疏密波，2/100 Hz，0.5~1.0 mA，20 min/d，14 d）。LequesneMG行为学量表评估大鼠膝关节功能、苏木精-伊红染色（HE）观察大鼠软骨细胞病理改变；透射电镜（TEM）观察大鼠软骨细胞超微结构形态、Western blotting检测TLR4、MyD88、NF-κBp65、II型胶原蛋白（COL2）、X型胶原蛋白（COL10）、Bcl-2关联X蛋白（Bax）、B淋巴细胞瘤-2蛋白（Bcl-2）、半胱氨酸天冬氨酸蛋白酶-3蛋白（Caspase-3）表达水平，实时荧光定量PCR法检测软骨组织TLR4、MyD88、NF-κB p65 mRNA表达水平；酶联免疫吸附试验（ELISA）检测各组大鼠血清中白细胞介素（IL）-1β、肿瘤坏死因子（TNF）-α水平。另取15只SPF级SD大鼠，随机分为空白组、模型组、抑制剂组（TAK-242）、电针组、假电针组（n=3），Western blotting检测高迁移率族蛋B1（HMGB1）及通路关键蛋白表达，并分析NF-κB p65核转位情况。结果与空白组比较，模型组大鼠LequesneMG评分升高，HE染色可见膝关节软骨细胞减少，细胞肿胀，细胞核固缩、消失，电镜下软骨细胞膜失去完整性，细胞核呈不规则形态，染色质固缩呈团块状，线粒体肿胀、嵴被破坏，TLR4/MyD88/NF-κB p65、COL10、Bax、Caspase-3蛋白及mRNA表达升高，COL2、Bcl-2表达降低，血清IL-1β、TNF-α水平升高（P<0.01）。与模型组比较，电针干预可显著降低LequesneMG评分，改善软骨组织结构损伤及细胞超微结构异常；下调TLR4、MyD88、NF-κB p65及Bax、Caspase-3表达，上调Bcl-2表达，同时降低血清IL-1β、TNF-α水平（P<0.01）。Western blotting结果显示，模型组大鼠软骨组织中HMGB1蛋白表达显著升高（P<0.01），并伴随NF-κBp65核转位增强；电针干预后HMGB1表达下降，NF-κB p65核内表达降低、胞质表达回升（P<0.01）。TLR4抑制剂组呈现相似变化趋势，而假电针组未见明显改善（P>0.05）。同时，TLR4、MyD88及NF-κB p65的mRNA表达变化趋势与蛋白水平一致。结论电针可能通过抑制HMGB1介导的TLR4/MyD88/NF-κB信号通路异常激活，减少NF-κB p65核转位，进而调节Bcl-2/Bax表达平衡，抑制线粒体依赖性软骨细胞凋亡过程，从而发挥抗炎及抗凋亡作用并改善KOA软骨损伤。

关键词: 膝关节骨关节炎, TLR4/MyD88/NF-κB信号通路, 电针, 凋亡, 膝关节软骨

Abstract:

Objective To investigate the effect of electroacupuncture (EA) on chondrocyte apoptosis in rats with knee osteoarthritis (KOA) and the underlying mechanism. Methods Twenty-seven SD rats were randomly divided into blank group, KOA model group, and EA group (n=9). Rat models of KOA were established by intra-articular injection of monosodium iodoacetate, and EA treatment was administered at the acupoints "Neixiyan", "Dubi", "Xuehai", and "Yanglingquan" (dense-sparse wave, 2/100 Hz, 0.5-1.0 mA, 20 min/day for 14 days). Knee function of the rats was assessed using Lequesne MG scale, and cartilage pathologies and ultrastructural changes were observed with HE staining and transmission electron microscopy. The protein expressions of TLR4, MyD88, NF-κB p65, COL2, COL10, Bax, Bcl-2, and caspase-3 and mRNA levels of TLR4, MyD88, and NF‑κB p65 were detected using Western blotting and RT-qPCR; serum levels of IL-1β and TNF‑α were determined with ELISA. Another 15 rats were randomized into blank control, model, TLR4 inhibitor (TAK-242), EA, and sham-EA groups (n=3) for analysis of HMGB1 and key pathway protein expressions and NF‑κB p65 nuclear translocation. Results The KOA rats showed increased Lequesne MG scores, obvious chondrocyte injuries, upregulated TLR4, MyD88, NF‑κB p65, COL10, Bax, and caspase-3 expressions, increased serum IL-1β and TNF‑α levels with decreased COL2 and Bcl-2 expressions. EA significantly reduced Lequesne MG scores, improved cartilage pathologies and reversed the abnormal changes in protein expressions and inflammatory cytokines. The KOA rats showed increased HMGB1 expression and enhanced NF‑κB p65 nuclear translocation, and EA treatment effectively decreased HMGB1 expression, reduced nuclear NF‑κB p65, and increased cytoplasmic NF‑κB p65. The TLR4 inhibitor produced similar effects, while sham EA produced no significant effect. Conclusion EA alleviates cartilage injury in KOA rats possibly by inhibiting HMGB1-mediated activation of TLR4/MyD88/NF‑κB signaling and NF‑κB p65 nuclear translocation to regulate Bcl-2/Bax balance and suppress mitochondria-dependent chondrocyte apoptosis.

Key words: knee osteoarthritis, TLR4/MyD88/NF-κB signaling pathway, electroacupuncture, apoptosis, knee cartilage

李春宁, 杨琪琪, 张振丰, 鲍亮, 姜天鑫, 张玉, 李飞. 电针通过调控TLR4/MyD88/NF-κB信号通路减轻膝关节骨关节炎大鼠膝关节软骨凋亡[J]. 南方医科大学学报, 2026, 46(8): 1886-1895.

Chunning LI, Qiqi YANG, Zhenfeng ZHANG, Liang BAO, Tianxin JIANG, Yu ZHANG, Fei LI. Electroacupuncture alleviates articular chondrocyte apoptosis in rats with knee osteoarthritis by regulating the TLR4/MyD88/NF-κB signaling pathway[J]. Journal of Southern Medical University, 2026, 46(8): 1886-1895.

图/表 9

表1 引物序列

Tab.1 Primer sequences for RT-qPCR

Gene	Amplicon size (bp)	Forward primer (5'→3')	Reverse primer (5'→3')
TLR4	188	CACCAGGAAGCTTGAATCCCT	ATCCAGCCACTGAAGTTCTGA
Myd88	178	CATACCCTTGGTCGCGCTTA	CCAGGCATCCAACAAACTGC
NF-κB p65	181	CATGGAGGTGGCGGTCTATC	CACAGCGTACATCAGGTGGT
GAPDH	78	TGGTGAAGCAGGCATCTGAG	TGAAGTCGCAGGAGACAACC

图1 各组大鼠造模后及干预后LequesneMG评分比较

Fig.1 Comparison of LequesneMG scores of the rats in the 3 groups after modeling and intervention (Mean±SD, n=9). **P<0.01 vs Control group,##P<0.05 vs Model group.

图2 HE染色各组大鼠膝关节软骨细胞病理结构比较

Fig.2 Pathological changes of knee articular chondrocytes in rats from different groups (HE staining, Scale bar=20 μm). Arrows indicate nuclear pyknosis, disappearance, and cell swelling.

图3 透射电镜下各组大鼠软骨核膜、染色质、线粒体的超微结构比较

Fig.3 Transmission electron microscopy showing ultrastructural changes of the chondral nucleus membrane, chromatin, and mitochondria of the rats. The blue arrow indicates the nuclear envelope, the red arrow indicates the mitochondria, and the green arrow indicates the chromatin.

图4 Western blotting检测三组大鼠膝关节软骨组织TLR4、MyD88、NF-κBp65、COL2、COL10、Bax、Bcl-2、Caspase-3蛋白表达水平

Fig.4 Western blotting for detecting protein expression levels of TLR4, MyD88, NF-κBp65, COL2, COL10, Bax, Bcl-2, and Caspase-3 in the knee joint cartilage of the rats (Mean±SD, n=3 ). **P<0.01 vs Control group, ##P<0.05 vs Model group.

图5 3组大鼠膝关节软骨组织TLR4、MyD88、NF-κB p65 mRNA表达水平比较

Fig.5 Comparison of TLR4, MyD88, and NF-κB p65 mRNA expression levels in knee joint cartilage tissues among the 3 groups (Mean±SD, n=3). **P<0.01 vs Control group,##P<0.05 vs Model group.

图6 各组大鼠血清中IL-1β、TNF-α表达比较

Fig.6 Comparison of serum IL-1β and TNF-α levels among the 3 groups (Mean±SD, n=9). **P<0.01 vs Control group, ##P<0.05 vs Model group.

图7 Western blotting检测大鼠膝关节软骨组织HMGB1、TLR4、MyD88蛋白表达水平以及NF-κB p65入核情况比较

Fig.7 Western blotting for detecting expression levels of HMGB1, TLR4, and MyD88 proteins and nuclear translocation of NF‑κB p65 in knee articular cartilage tissues of the rats (Mean±SD, n=3). **P<0.01 vs Control group, ##P<0.05 vs Model group.

图8 5组大鼠膝关节软骨组织TLR4、MyD88、NF-κB p65 mRNA表达水平比较

Fig.8 Comparison of TLR4, MyD88, and NF-κB p65 mRNA expression levels in knee joint cartilage tissue among five groups of rats (Mean±SD, n=3). **P<0.01 vs Control group, ##P<0.05 vs Model group.

参考文献 36

[1]	Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the Global Burden of Disease 2010 study[J]. Ann Rheum Dis, 2014, 73(7): 1323-30. doi：10.1136/annrheumdis-2013-204763
[2]	Racine J, Aaron RK. Pathogenesis and epidemiology of osteoarthritis[J]. R I Med J, 2013,96(3):19-22.
[3]	Hwang HS, Kim HA. Chondrocyte apoptosis in the pathogenesis of osteoarthritis[J]. Int J Mol Sci, 2015, 16(11): 26035-54. doi：10.3390/ijms161125943
[4]	Miao GQ, Zang XH, Hou HG, et al. Bax targeted by miR-29a regulates chondrocyte apoptosis in osteoarthritis[J]. BioMed Res Int, 2019, 2019: 1434538. doi：10.1155/2019/1434538
[5]	Scanzello CR, Plaas A, Crow MK. Innate immune system activation in osteoarthritis: is osteoarthritis a chronic wound?[J]. Curr Opin Rheumatol, 2008, 20(5): 565-72. doi：10.1097/bor.0b013e32830aba34
[6]	杨琪琪, 姜天鑫, 李春宁, 等. 电针治疗膝关节骨关节炎慢性疼痛患者的疗效及对中枢敏化的影响[J/OL].中国针灸, [2026-05-11].
[7]	Melzack R, Wall PD. Pain mechanisms: a new theory[J]. Science, 1965, 150(3699): 971-9. doi：10.1126/science.150.3699.971
[8]	Duan B, Cheng LZ, Bourane S, et al. Identification of spinal circuits transmitting and gating mechanical pain[J]. Cell, 2014, 159(6): 1417-32. doi：10.1016/j.cell.2014.11.003
[9]	李杨乐, 杨锋, 樊静杰, 等. 电针对膝骨关节炎大鼠脊髓背角CB2R、p-P38和p-ERK表达的影响[J]. 中国中医药信息杂志, 2022, 29(7): 60-6.
[10]	鲍哲明, 单青, 李晨, 等. 碘乙酸钠大鼠骨关节炎模型骨微结构研究[J]. 中国骨质疏松杂志, 2022, 28(2): 210-4, 219.
[11]	Lequesne MG, Samson M. Indices of severity in osteoarthritis for weight bearing joints[J]. J Rheumatol Suppl, 1991, 27: 16-8.
[12]	中国针灸学会. 实验动物常用穴位名称与定位第2部分: 大鼠[J]. 针刺研究, 2021, 46(4): 351-2.
[13]	Lequesne MG. The algofunctional indices for hip and knee osteoarthritis[J]. J Rheumatol, 1997, 24 4:779-81.
[14]	Dong JB, Liao Y, Wu BH. TAK-242 ameliorates epileptic symptoms in mice by inhibiting the TLR4/NF‑κB signaling pathway[J]. Ann Transl Med, 2022, 10(14): 795. doi：10.21037/atm-22-2707
[15]	李益军, 梁兴森, 方细霞, 等. 电针与关节液炎症因子及关节运动功能恢复的相关性研究[J]. 时珍国医国药, 2024, 35(6): 1415-9. doi：10.3969/j.issn.1008-0805.2024.06.31
[16]	郑祥, 高颂爱, 尤浩, 等. 电针可改善骨关节炎大鼠的关节炎症和运动功能: 基于调控Wnt-7B/β-catenin信号通路[J]. 南方医科大学学报, 2023, 43(4): 590-6.
[17]	陈蔚, 李恒聪, 万红叶, 等. 电针对膝关节骨关节炎大鼠滑膜炎性反应期自发痛及后期触诱发痛的影响[J]. 中国针灸, 2022, 42(12): 1385-93. doi：10.13703/j.0255-2930.20220526-k0006
[18]	周欣华, 杨琪琪, 李蔚然, 等. 电针调控PI3K/Akt/mTOR通路对膝关节骨关节炎大鼠膝关节滑膜组织自噬的影响[J]. 针刺研究, 2026, 51(1): 59-67.
[19]	周巧, 刘健, 万磊, 等. 新风胶囊抑制软骨细胞炎症和细胞外基质降解: 基于调控miR-502-5p/TRAF2/NF-κB轴[J]. 南方医科大学学报, 2024, 44(1): 108-18. doi：10.12122/j.issn.1673-4254.2024.01.13
[20]	Jørgensen AEM, Agergaard J, Schjerling P, et al. The regional turnover of cartilage collagen matrix in late-stage human knee osteoarthritis[J]. Osteoarthritis Cartilage, 2022, 30(6): 886-95. doi：10.1016/j.joca.2022.03.007
[21]	Yang JZ, Chen DL, He Q, et al. Arctiin alleviates knee osteoarthritis by suppressing chondrocyte oxidative stress induced by accumulated iron via AKT/NRF2/HO-1 signaling pathway[J]. Sci Rep, 2024, 14: 31935. doi：10.1038/s41598-024-83383-7
[22]	Zhang JM, Hao XX, Chi RM, et al. Moderate mechanical stress suppresses the IL-1β-induced chondrocyte apoptosis by regulating mitochondrial dynamics[J]. J Cell Physiol, 2021, 236(11): 7504-15. doi：10.1002/jcp.30386
[23]	Millerand M, Berenbaum F, Jacques C. Danger signals and inflammaging in osteoarthritis[J]. Clin Exp Rheumatol, 2019, 37 Suppl 120(5): 48-56.
[24]	Kapoor M, Martel-Pelletier J, Lajeunesse D, et al. Role of proinflammatory cytokines in the pathophysiology of osteoarthritis[J]. Nat Rev Rheumatol, 2011, 7(1): 33-42. doi：10.1038/nrrheum.2010.196
[25]	Zhang X, Hsueh MF, Huebner JL, et al. TNF-α carried by plasma extracellular vesicles predicts knee osteoarthritis progression[J]. Front Immunol, 2021, 12: 758386. doi：10.3389/fimmu.2021.758386
[26]	Tseng HC, Wu MR, Lee CH, et al. Differentiation capacity of bone marrow-derived rat mesenchymal stem cells from DsRed and cre transgenic cre/loxP models[J]. Cells, 2022, 11(17): 2769. doi：10.3390/cells11172769
[27]	Chen L, Wei K, Li J, et al. Integrated analysis of LncRNA-mediated CeRNA network in calcific aortic valve disease[J]. Cells, 2022, 11(14): 2204. doi：10.3390/cells11142204
[28]	Zhang Y, Zeng Y. Curcumin reduces inflammation in knee osteoarthritis rats through blocking TLR4/MyD88/NF-κB signal pathway[J]. Drug Dev Res, 2019, 80(3): 353-9. doi：10.1002/ddr.21509
[29]	Xu XT, Li NP, Wu YR, et al. Zhuifeng tougu capsules inhibit the TLR4/MyD88/NF‑κB signaling pathway and alleviate knee osteoarthritis: in vitro and in vivo experiments[J]. Front Pharmacol, 2022, 13: 951860. doi：10.3389/fphar.2022.951860
[30]	庄丽华, 詹松华, 杨烁慧, 等. 电针通过调节TLR4/MyD88/NF-κb信号通路改善缺血性脑卒中损伤研究现状[J]. 中华中医药学刊, 2019, 37(9): 2182-5.
[31]	晏黎, 饶亚华, 黄伟, 等. 损伤相关分子模式与组织修复[J]. 中国免疫学杂志, 2022, 38(7): 872-7.
[32]	邵建彬, 王霞, 徐华洲, 等. 芪苓通络方抑制TLR4/MyD88/NF-κB信号通路改善特发性膜性肾病大鼠肾损伤[J]. 中国实验方剂学杂志, 2022, 28(4): 100-8.
[33]	Sun FF, Hu PF, Xiong Y, et al. Tricetin protects rat chondrocytes against IL-1β-induced inflammation and apoptosis[J]. Oxid Med Cell Longev, 2019, 2019(1): 4695381. doi：10.1155/2019/4695381
[34]	D'Arcy MS. Cell death: a review of the major forms of apoptosis, necrosis and autophagy[J]. Cell Biol Int, 2019, 43(6): 582-92. doi：10.1002/cbin.11137
[35]	李亚楠, 倪娟, 方禹舜, 等. 姜黄素通过调控脂多糖诱导的炎症抑制软骨细胞凋亡[J]. 中成药, 2021, 43(7): 1904-8. doi：10.3969/j.issn.1001-1528.2021.07.042
[36]	Zhang YB, Cai WS, Han GT, et al. Panax notoginseng saponins prevent senescence and inhibit apoptosis by regulating the PI3K-AKT-mTOR pathway in osteoarthritic chondrocytes[J]. Int J Mol Med, 2020, 49(3):30.

电针通过调控TLR4/MyD88/NF-κB信号通路减轻膝关节骨关节炎大鼠膝关节软骨凋亡

Electroacupuncture alleviates articular chondrocyte apoptosis in rats with knee osteoarthritis by regulating the TLR4/MyD88/NF-κB signaling pathway

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