文献类型：期刊文献

中文题名：电热针靶向针刺对颞下颌关节骨关节炎模型大鼠TLR4/NF-κB信号通路的影响

英文题名：Effects of electrothermal acupuncture targeted intervention on the TLR4/NF-κB signaling pathway in temporomandibular joint osteoarthritis model rats

作者：王银平[1];樊晶[1];强胜林[2]

第一作者：王银平

机构：[1]甘肃中医药大学针灸推拿学院,甘肃兰州730101;[2]甘肃中医药大学附属医院创伤骨科,甘肃兰州730020

第一机构：甘肃中医药大学针灸推拿学院

年份：2025

卷号：42

期号：6

起止页码：9

中文期刊名：甘肃中医药大学学报

外文期刊名：Journal of Gansu University of Chinese Medicine

基金：甘肃省自然科学基金项目(21JR7RA582)。

语种：中文

中文关键词：颞下颌关节骨关节炎;电热针;靶向针刺;Toll样受体4/核因子-κB信号通路;炎症因子;大鼠;实验研究

外文关键词：temporomandibular joint osteoarthritis;electrothermal acupuncture;targeted acupuncture;TLR4/NF-κB signaling pathway;inflammatory factors;rats;experimental study

摘要：目的基于Toll样受体4/核因子-κB(TLR4/NF-κB)信号通路,探讨电热针靶向针刺干预颞下颌关节骨关节炎(TMJOA)模型大鼠的效应机制。方法将50只Wistar雄性大鼠采用随机数字表法分为空白组、模型组、电热针组、温针灸组和普通针刺组,每组10只。于大鼠颞下颌关节上腔注射碘乙酸钠溶液复制TMJOA模型,各干预组给予相应方法进行干预。采用Von Frey测痛仪测定各组大鼠摆头阈值,通过苏木精-伊红(HE)染色法观察各组大鼠颞下颌关节髁突组织病理学变化,通过酶联免疫吸附测定(ELISA)法检测各组大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的含量,采用实时荧光定量聚合酶链式反应法、Western Blot法检测各组大鼠颞下颌关节髁突软骨组织中TLR4、NF-κB p65 mRNA及蛋白的表达。结果与空白组比较,TMJOA模型大鼠摆头阈值均明显降低,差异有统计学意义(P<0.01);与模型组比较,电热针组大鼠血清IL-1β、IL-6、TNF-α含量均明显降低(P<0.01),温针灸组和普通针刺组大鼠血清IL-6、TNF-α含量均明显降低(P<0.05或P<0.01),且电热针组各项指标均明显低于温针灸组和普通针刺组(P<0.05或P<0.01);与模型组比较,电热针组、温针灸组、普通针刺组大鼠颞下颌关节髁突软骨组织NF-κB p65、TLR4 mRNA及蛋白相对表达量均明显降低(P<0.01),且电热针组均明显低于温针灸组和普通针刺组(P<0.05或P<0.01)。结论电热针靶向针刺可通过抑制TMJOA模型大鼠颞下颌关节髁突软骨组织中TLR4/NF-κB信号通路的过度活化,下调该通路下游炎症因子(TNF-α、IL-1β、IL-6)的表达,从而减轻这些炎症因子对软骨细胞的持续刺激与破坏,延缓TMJOA病变进程。
Objective To investigate the mechanism of electrothermal acupuncture targeted intervention in a rat model of temporomandibular joint osteoarthritis(TMJOA)based on the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)signaling pathway.Methods 50 male Wistar rats were randomly divided into 5 groups(n=10 per group):blank control group,model group,electrothermal acupuncture group,warm acupuncture group,and conventional acupuncture group.The TMJOA model was established by injecting sodium iodoacetate solution into the upper cavity of the temporomandibular joint.Each intervention group received the corresponding treatment.The head-shaking threshold was measured using a Von Frey pain measurement device.Histopathological changes in the temporomandibular joint condylar cartilage were observed via hematoxylin and eosin(HE)staining.Serum levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),and interleukin-6(IL-6)were detected using enzyme-linked immunosorbent assay(ELISA).The mRNA and protein expression levels of TLR4 and NF-κB p65 in the temporomandibular joint condylar cartilage were measured using real-time quantitative polymerase chain reaction(RT-PCR)and Western blot analysis.Results Compared with the blank control group,the head-shaking thresholds of TMJOA model rats were significantly lower(P<0.01).Compared with the model group,the serum levels of IL-1β,IL-6,and TNF-αin the electrothermal acupuncture group were significantly lower(P<0.01),while the warm acupuncture and conventional acupuncture groups showed significantly reduced serum levels of IL-6 and TNF-α(P<0.05 or P<0.01).Moreover,the electrothermal acupuncture group exhibited significantly lower values for all indicators compared to the warm acupuncture and conventional acupuncture groups(P<0.05 or P<0.01).Compared with the model group,the relative mRNA and protein expression levels of NF-κB p65 and TLR4 in the temporomandibular joint condylar cartilage were significantly lower in the electrothermal acupuncture,warm acupuncture,and conventional acupuncture groups(P<0.01),with the electrothermal acupuncture group showing significantly lower le-vels than the warm acupuncture and conventional acupuncture groups(P<0.05 or P<0.01).Conclusion Electrothermal acupuncture targeted intervention can inhibit the overactivation of the TLR4/NF-κB signaling pathway in the temporomandibular joint condylar chondrocytes of TMJOA model rats,downregulate the expression of downstream inflammatory factors(such as TNF-α,IL-1β,and IL-6),thereby reducing the sustained stimulation and damage to chondrocytes caused by these inflammatory factors and delaying the progression of TMJOA.