Zhang Qi, Wang Xiang, Yan Guifang, Lei Juan, Zhou Yu, Wu Lei, Wang Ting, Zhang Xiao, Ye Duyun, Li Yongsheng
Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.
Cell Physiol Biochem. 2018;45(4):1377-1389. doi: 10.1159/000487563. Epub 2018 Feb 15.
BACKGROUND/AIMS: This study aimed to explore the metabololipidome in mice upon cupping treatment.
A nude mouse model mimicking the cupping treatment in humans was established by administrating four cupping sets on the back skin for 15 minutes. UPLC-MS/ MS was performed to determine the PUFA metabolome in mice skin and blood before and after cupping treatment. The significantly changed lipids were administered in macrophages to assess the production of pro-inflammatory cytokines IL-6 and TNF-α by ELISA.
The anti-inflammatory lipids, e.g. PGE1, 5,6-EET, 14,15-EET, 10S,17S-DiHDoHE, 17R-RvD1, RvD5 and 14S-HDoHE were significantly increased while pro-inflammatory lipids, e.g. 12-HETE and TXB2 were deceased in the skin or plasma post cupping treatment. Cupping treatment reversed the LPS-stimulated IL-6 and TNF-α expression in mouse peritoneal exudates. Moreover, 5,6-EET, PGE1 decreased the level of TNF-α, while 5,6-EET, 5,6-DHET downregulated IL-6 production in macrophages. Importantly, 14,15-EET and 14S-HDoHE inhibited both IL-6 and TNF-α induced by lipopolysaccharide (LPS). 17-RvD1, RvD5 and PGE1 significantly reduced the LPS-initiated TNF-α, while TXB2 and 12-HETE further upregulated the LPS-enhanced IL-6 and TNF-α expression in macrophages.
Our results reveal the identities of anti-inflammatory versus pro-inflammatory metabolipidome and suggest the potential therapeutic mechanism of cupping treatment.
背景/目的：本研究旨在探索拔罐治疗后小鼠的代谢脂质组。
通过在裸鼠背部皮肤进行四组拔罐治疗15分钟，建立模拟人类拔罐治疗的裸鼠模型。采用超高效液相色谱-质谱/质谱法测定拔罐治疗前后小鼠皮肤和血液中的多不饱和脂肪酸代谢组。将显著变化的脂质作用于巨噬细胞，通过酶联免疫吸附测定法评估促炎细胞因子白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的产生。
拔罐治疗后，皮肤或血浆中抗炎脂质如前列腺素E1（PGE1）、5,6-环氧二十碳三烯酸（5,6-EET）、14,15-EET、10S,17S-二氢二十二碳六烯酸（10S,17S-DiHDoHE）、17R-消退素D1（17R-RvD1）、消退素D5（RvD5）和14S-氢二十二碳六烯酸（14S-HDoHE）显著增加，而促炎脂质如12-羟基二十碳四烯酸（12-HETE）和血栓素B2（TXB2）减少。拔罐治疗可逆转脂多糖刺激的小鼠腹腔渗出液中IL-6和TNF-α的表达。此外，5,6-EET、PGE1可降低TNF-α水平，而5,6-EET、5,6-二氢环氧二十碳三烯酸（5,6-DHET）可下调巨噬细胞中IL-6的产生。重要的是，14,15-EET和14S-HDoHE可抑制脂多糖（LPS）诱导的IL-6和TNF-α。17-RvD1、RvD5和PGE1可显著降低LPS引发的TNF-α，而TXB2和12-HETE则进一步上调LPS增强的巨噬细胞中IL-6和TNF-α的表达。
我们的结果揭示了抗炎与促炎代谢脂质组的特征，并提示了拔罐治疗的潜在治疗机制。
