Ophthalmology Department of Traditional Chinese Medicine, The First Clinical Medical College, Nanjing University of Traditional Chinese Medicine, Nanjing City, Jiangsu Province 210023, China.
Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing City, Jiangsu Province 210029, China.
Oxid Med Cell Longev. 2021 Apr 9;2021:6673610. doi: 10.1155/2021/6673610. eCollection 2021.
We tried to investigate whether electroacupuncture (EA) can reduce inflammation of dry eye disease (DED) by regulating 7nAChR and inhibiting the NF-B signaling pathway.
Healthy New Zealand white rabbits were treated with scopolamine hydrobromide (Scop) for 21 consecutive days to establish the DED animal model. After 21 days, EA, fluorometholone (Flu), and 7nAChR antagonist (-BGT) treatments were performed, and the Scop injection was continued until day 35. During treatment, the fluorescence staining of the corneal epithelium and the level of tear flow were observed. The influence of EA on the LG pathology and inflammatory factors ACh, 7nAChR, and NF-B was detected using the LG histopathology, transmission electron microscopy (TEM), cytokine protein chip technology, enzyme-linked immunosorbent assay (ELISA), and Western blot.
The EA stimulation can reduce the corneal epithelial damage and repair epithelial cell ultrastructure, promote the tear secretion, relieve the LG atrophy and decrease lipid droplet accumulation in LG acinar cell, and reduce the levels of inflammatory cytokines (i.e., IL-1, MIP-1b, TNF-, and IL-8) in the LG. The protective effect of EA on the inflammation and the ocular surface is similar to the corticosteroid Flu. EA and Flu can upregulate the expression of the 7nAChR and downregulate the expression of NF-B. The 7nAChR antagonist -BGT can reverse the protective effect of EA on the LG and the inhibitory effect on the NF-B pathway and the expression of inflammatory factors but cannot affect the expression of Flu on the NF-B pathway and inflammatory factors.
These results prove that EA can alleviate DEDs by stimulating the acupoints around the eyes. These beneficial effects are related to the upregulation of 7nAChR and the downregulation of NF-B in the LG. The protective effect of LG is mediated through the anti-inflammatory pathway mediated by 7nAChR. EA can reduce the NF-B P65 nuclear transcription and reduce inflammatory factors by regulating 7nAChR. This expression indicates that the 7nAChR/NF-B signaling pathway may serve as a potential therapeutic target for EA to treat DEDs.
本研究旨在探讨电针对干眼症（DED）的抗炎作用是否与调节 7 型烟碱乙酰胆碱受体（7nAChR）和抑制 NF-B 信号通路有关。
采用氢溴酸东莨菪碱（Scop）连续滴眼 21 天建立兔 DED 模型，造模成功后，电针、氟米龙（Flu）和 7nAChR 拮抗剂（-BGT）分别干预 14 天，同时继续给予 Scop 滴眼至第 35 天。观察角膜荧光素染色及泪液分泌量，光镜、透射电镜观察结膜组织病理学变化，酶联免疫吸附法（ELISA）检测泪液中 ACh、7nAChR 及 NF-B 表达，免疫组织化学法和蛋白芯片技术检测结膜组织中 NF-B P65 核转录因子的表达。
电针刺激能减轻角膜上皮损伤，修复上皮细胞超微结构，促进泪液分泌，减轻结膜组织萎缩，减少杯状细胞内脂滴堆积，降低结膜组织中促炎因子白细胞介素 1（IL-1）、巨噬细胞炎性蛋白 1β（MIP-1β）、肿瘤坏死因子-α（TNF-α）和白细胞介素 8（IL-8）的水平。电针和 Flu 对炎症和眼表的保护作用与皮质激素 Flu 相似。电针和 Flu 能上调 7nAChR 的表达，下调 NF-B 的表达。7nAChR 拮抗剂 -BGT 能逆转电针的保护作用和对 NF-B 通路及炎症因子的抑制作用，但不能影响 Flu 对 NF-B 通路及炎症因子的表达。
电针通过刺激眼周穴位减轻 DED，其有益作用与上调结膜组织中 7nAChR 及下调 NF-B 有关。该保护作用是通过 7nAChR 介导的抗炎通路发挥的。电针可能通过调节 7nAChR 减少 NF-B P65 核转录和炎症因子的表达来发挥作用。这些结果表明，7nAChR/NF-B 信号通路可能是电针治疗 DED 的潜在治疗靶点。
