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. 2018 Apr 25;8:6523. doi: 10.1038/s41598-018-24654-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Local injection of sodium cromolyn into ST36 did not inhibit the analgesic effect caused by A1 receptor activation at this acupoint. The pain threshold was normalised according to the pre-modelling pain threshold; the data are presented as the mean ± s.e.m. On day 1, the AA model was established; however, the pre-modelling pain threshold was measured before establishing the model. On day 3, the post-modelling pain threshold was measured first, and the post-treatment pain threshold was measured 20 min after the treatment. For the ACU group, acupuncture was performed at ST36 for 20 min. For the A1R group, CCPA solution was injected locally at the acupoint. For the CRO + A1R group, sodium cromolyn was injected locally at the acupoint 5 min before the injection of CCPA. *vs ACU group, P < 0.05.