Chen Wei, Li Heng-Cong, Wan Hong-Ye, Liu Yi-Han, Jing Xiang-Hong, Zhang Xiao-Ning, He Wei
Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing 100700, China.
Zhongguo Zhen Jiu. 2022 Dec 12;42(12):1385-93. doi: 10.13703/j.0255-2930.20220526-k0006.
To observe the effect of electroacupuncture (EA) on pain behavior, synovial inflammatory response and demyelination of saphenous nerve in the rats modeled with knee osteoarthritis (KOA) and explore the effect mechanism of EA for reliving allodynia.
Eighty-four male SD rats were randomly divided into a control group, a model group and an EA group, 28 rats in each one. Intra-articular injection of sodium monoiodoacetate (MIA) was administered in right knee joint of each rat in the model group and the EA group to establish the KOA model. In the EA group, separately, on day 5, 7 and 9 after modeling, EA was applied at "Zusanli" (ST 36) and "Yanglingquan" (GB 34) on the right side, with disperse-dense wave (2 Hz/15 Hz), 1 mA in current intensity, for 30 min in one intervention, once a day, and 3 interventions were required. On the 9th day after modeling, the weight-bearing rate was calculated for the affected limbs of the rats in each group, the synovial morphological changes were observed using HE and Masson staining, flow cytometry was adopted to detect the synovial immunocyte counts, and MSD multi-spot assay was used to detected the synovial inflammatory cytokine content. On the 14th day after modeling, the hind-paw mechanical withdrawal threshold was observed in each group and the ultrastructure of the saphenous nerve was observed under transmission electron microscopy.
On the 9th day after modeling, compared with the control group, the weight-bearing rate of the affected limb was reduced (<0.01), the synovial hyperplasia, inflammatory cell infiltration and synovial fibrosis occurred in the affected limb; the counts of synovial CD11b cells and M1 macrophages (CD11bCD86) were increased (<0.01), the contents of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, IL-10 and IL-13 in the synovial tissue were elevated (<0.01, <0.05) for the rats of the model group. Compared with the model group, the weight-bearing rate of the affected limb was increased (<0.05), the synovial hyperplasia, inflammatory cell infiltration and synovial fibrosis were mitigated, the counts of CD11b cells and M1 macrophages (CD11bCD86) in the synovial tissue, and the contents of TNF-α and IL-6 were reduced (<0.01, <0.05) in the EA group. On the 14th day after modeling, the hind-paw mechanical withdrawal threshold was reduced in the model group when compared with the control group (<0.01), and it was increased in the EA group when compared with the model group (<0.05). Besides, in the model group, obviously, the myelin sheath structure was destroyed, the myelin layer was disintegrated and loosened, the axon was extruded or the layer thicken and cracked. Compared with the model group, the injury of saphenous nerve was alleviated remarkably in the EA group.
The intervention with EA may attenuate the synovial inflammatory response and the injury of saphenous nerve in the affected limb of the rat with KOA, so that the spontaneous pain during the synovial inflammatory response stage and allodynia at the later stage are relieved.
观察电针对膝骨关节炎(KOA)模型大鼠疼痛行为、滑膜炎症反应及隐神经脱髓鞘的影响,探讨电针缓解异常性疼痛的作用机制。
将84只雄性SD大鼠随机分为对照组、模型组和电针组,每组28只。模型组和电针组大鼠右膝关节腔内注射单碘乙酸钠(MIA)建立KOA模型。电针组在造模后第5、7、9天,分别针刺右侧“足三里”(ST 36)和“阳陵泉”(GB 34),采用疏密波(2 Hz/15 Hz),电流强度1 mA,每次干预30 min,每天1次,共干预3次。造模后第9天,计算各组大鼠患侧肢体负重率,采用HE和Masson染色观察滑膜形态学变化,采用流式细胞术检测滑膜免疫细胞计数,采用MSD多斑点分析法检测滑膜炎症细胞因子含量。造模后第14天,观察各组大鼠后足机械缩足阈值,并在透射电镜下观察隐神经超微结构。
造模后第9天,与对照组比较,模型组大鼠患侧肢体负重率降低(<0.01),患侧滑膜增生、炎性细胞浸润及滑膜纤维化;滑膜CD11b细胞及M1巨噬细胞(CD11bCD86)计数增加(<0.01),滑膜组织中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6、IL-1β、IL-10及IL-13含量升高(<0.01,<0.05)。与模型组比较,电针组大鼠患侧肢体负重率升高(<0.05),滑膜增生、炎性细胞浸润及滑膜纤维化减轻,滑膜组织中CD11b细胞及M1巨噬细胞(CD11bCD86)计数及TNF-α、IL-6含量降低(<0.01,<0.05)。造模后第14天,与对照组比较,模型组大鼠后足机械缩足阈值降低(<0.01),与模型组比较,电针组大鼠后足机械缩足阈值升高(<0.05)。此外,模型组可见明显的髓鞘结构破坏,髓鞘层崩解、疏松,轴突受压或增厚、断裂。与模型组比较,电针组隐神经损伤明显减轻。
电针干预可减轻KOA大鼠患侧肢体滑膜炎症反应及隐神经损伤,从而缓解滑膜炎症反应期的自发痛及后期的异常性疼痛。