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电针对足三里穴(ST36)的刺激通过触发局部白细胞介素-10(IL-10)的产生和抑制 p38 丝裂原活化蛋白激酶(p38 MAPK)的激活抑制变应性接触性皮炎的炎症。

Electro-Acupuncture at Zusanli Acupoint (ST36) Suppresses Inflammation in Allergic Contact Dermatitis Via Triggering Local IL-10 Production and Inhibiting p38 MAPK Activation.

机构信息

Department of Pathogen Biology, College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, 430065, China.

College of Acupuncture and Moxibustion, Hubei University of Chinese Medicine, Wuhan, 430065, China.

出版信息

Inflammation. 2017 Aug;40(4):1351-1364. doi: 10.1007/s10753-017-0578-5.

Abstract

Acupuncture has shown beneficial effect in the treatment of multiple dermatologic conditions including dermatitis, pruritus, urticaria, and hyperhidrosis; however, the detailed mechanisms are still kept unclear. This study aimed to investigate if electro-acupuncture (EA) treatment prevents 2,4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis (ACD) in rats and explore its underlying mechanisms. ACD was induced by sensitizing and challenging with DNFB topically. Rats were treated daily following bilateral subcutaneous stimulation of EA at Zusanli acupoint (ST36) for 1 week. Ear swelling and serum IgE levels were measured. The ear biopsies were obtained for histology. Inflammatory cytokines on the dermatological ear and local acupoint tissue were assayed. Spleen lymphocytes and the homogenized supernatant of local acupuncture area were used to co-culture for flow cytology and immune analysis, respectively. EA treatment at ST36 notably inhibited ear swelling and inflammatory cell infiltration on DNFB-induced ACD. EA also decreased serum IgE concentrations and alleviated the production of inflammatory cytokines in dermatological ear. Additionally, EA treatment attenuated the percentage of CD4IFN-γ and CD4IL-4 T cells associated with ACD. Interestingly, secretion of interleukin (IL)-10 in the local acupoint tissue following EA stimulation was increased and showed suppressive function when co-cultured with the spleen lymphocytes from DNFB group. Lastly, EA treatment demonstrably suppressed p38 MAPK activation in DNFB-treated rats. Our findings suggest that EA treatment at ST36 may ameliorate inflammation associated with DNFB-induced ACD via triggering local IL-10 production and inhibiting p38 MAPK activation, which provide an alternative and promising therapy for ACD.

摘要

针刺在治疗多种皮肤病方面显示出有益的效果,包括皮炎、瘙痒症、荨麻疹和多汗症;然而,其详细机制仍不清楚。本研究旨在探讨电针对 2,4-二硝基氟苯(DNFB)诱导的变应性接触性皮炎(ACD)大鼠的预防作用,并探讨其潜在机制。通过用 DNFB 进行局部致敏和激发来诱导 ACD。在双侧足三里穴位(ST36)进行皮下刺激后,每天对大鼠进行治疗,持续 1 周。测量耳肿胀和血清 IgE 水平。获取耳部活检以进行组织学检查。在皮肤病耳部和局部穴位组织上测定炎症细胞因子。将脾淋巴细胞和局部针刺区域的匀浆上清液分别用于共培养进行流式细胞术和免疫分析。ST36 处的电针对 DNFB 诱导的 ACD 引起的耳肿胀和炎症细胞浸润有明显抑制作用。电针还降低了血清 IgE 浓度,并减轻了皮肤病耳部炎症细胞因子的产生。此外,电针治疗还减弱了与 ACD 相关的 CD4IFN-γ和 CD4IL-4 T 细胞的比例。有趣的是,电针刺激后局部穴位组织中白细胞介素(IL)-10 的分泌增加,并在与来自 DNFB 组的脾淋巴细胞共培养时显示出抑制作用。最后,电针治疗明显抑制了 DNFB 处理大鼠中 p38 MAPK 的激活。我们的研究结果表明,ST36 处的电针治疗可能通过触发局部 IL-10 产生和抑制 p38 MAPK 激活来改善与 DNFB 诱导的 ACD 相关的炎症,为 ACD 提供了一种替代和有前途的治疗方法。

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