Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, China.
Department of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, China.
Acupunct Med. 2023 Jun;41(3):163-174. doi: 10.1177/09645284221107684. Epub 2022 Jul 1.
To detect the role of dopamine in the anti-inflammatory effect of electroacupuncture (EA) at ST36 in a mouse model of chronic obstructive pulmonary disease (COPD).
Twenty-eight male BALB/c mice were randomly divided into the control group, model group, sham EA (sham) group or ST36 EA (ST36) group in a 1:1:1:1 ratio ( = 7 each). The COPD mouse model was established through cigarette smoke (CS) exposure for 12 weeks. During the last 2 weeks, EA was applied at a sham point location or ST36 before CS exposure. Lung function, histopathological changes, inflammatory cell counts in bronchoalveolar lavage fluid (BALF), inflammatory cytokines in BALF, plasma, lung tissue homogenate (LTH), and plasma dopamine levels were detected in the different groups. Furthermore, the role of different dopamine receptors was explored through intraperitoneal injections of non-specific dopamine receptor antagonist chlorpromazine, specific dopamine D1 receptor antagonist SCH 23390 and specific dopamine D2 receptor antagonist eticlopride hydrochloride prior to ST36 EA and CS exposure.
EA at ST36 improved lung function, alleviated lung and systemic inflammatory responses by reducing inflammatory cells and cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-8 and IL-1β in BALF, plasma and lung tissue in this COPD mouse model. Plasma dopamine was greatly increased after EA at ST36, negatively correlated with lung histological lesions and inflammatory cytokine levels, and positively correlated with mice body weight and lung function indicators. Chlorpromazine and eticlopride hydrochloride inhibited the anti-inflammatory effect of EA at ST36, while SCH 23390 showed no neutralizing effect.
EA at ST36 could alleviate inflammation in this mouse model of COPD through the dopamine D2 receptor pathway.
检测多巴胺在电针（EA）刺激 ST36 穴对慢性阻塞性肺疾病（COPD）小鼠模型抗炎作用中的作用。
28 只雄性 BALB/c 小鼠随机分为对照组、模型组、假电针（假）组或 ST36 电针（ST36）组，比例为 1:1:1:1（=7 只/组）。通过香烟烟雾（CS）暴露 12 周建立 COPD 小鼠模型。在 CS 暴露前的最后 2 周，在假点位置或 ST36 进行 EA。检测各组小鼠的肺功能、组织病理学变化、支气管肺泡灌洗液（BALF）中的炎症细胞计数、BALF、血浆、肺组织匀浆（LTH）中的炎症细胞因子和血浆多巴胺水平。此外，在 ST36 EA 和 CS 暴露前通过腹腔注射非特异性多巴胺受体拮抗剂氯丙嗪、特异性多巴胺 D1 受体拮抗剂 SCH 23390 和特异性多巴胺 D2 受体拮抗剂盐酸依托必利，探讨不同多巴胺受体的作用。
ST36 电针可改善肺功能，减轻肺部和全身炎症反应，减少 BALF、血浆和肺组织中的炎症细胞因子 TNF-α、IL-8 和 IL-1β等。COPD 小鼠模型。ST36 电针后血浆多巴胺水平显著升高，与肺组织学病变和炎症细胞因子水平呈负相关，与小鼠体重和肺功能指标呈正相关。氯丙嗪和盐酸依托必利抑制了 ST36 电针的抗炎作用，而 SCH 23390 则没有中和作用。
ST36 电针通过多巴胺 D2 受体途径可减轻该 COPD 小鼠模型的炎症反应。
