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首页> 外文期刊>Cellular Physiology and Biochemistry >Anti- Versus Pro-Inflammatory Metabololipidome Upon Cupping Treatment
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Anti- Versus Pro-Inflammatory Metabololipidome Upon Cupping Treatment

机译:拔罐治疗后抗炎性代谢脂质脂组

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Background/Aims This study aimed to explore the metabololipidome in mice upon cupping treatment. Methods 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. Results 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. Conclusion Our results reveal the identities of anti-inflammatory versus pro-inflammatory metabolipidome and suggest the potential therapeutic mechanism of cupping treatment.
机译:背景/目的本研究旨在研究拔罐治疗后小鼠体内的脂质脂组。方法通过在背部皮肤上施用四个拔罐器15分钟,建立一个模拟人拔罐的裸鼠模型。进行UPLC-MS / MS测定拔罐治疗前后小鼠皮肤和血液中的PUFA代谢组。在巨噬细胞中施用明显改变的脂质,以通过ELISA评估促炎细胞因子IL-6和TNF-α的产生。结果抗炎脂质,例如。 PGE1、5,6-EET,14,15-EET,10S,17S-DiHDoHE,17R-RvD1,RvD5和14S-HDoHE显着增加,而促炎性脂质例如拔罐后皮肤或血浆中12-HETE和TXB2死亡。拔罐处理逆转了小鼠腹膜渗出液中LPS刺激的IL-6和TNF-α表达。此外,5,6-EET,PGE1降低了TNF-α的水平,而5,6-EET,5,6-DHET下调了巨噬细胞的IL-6产生。重要的是,14,15-EET和14S-HDoHE抑制由脂多糖(LPS)诱导的IL-6和TNF-α。 17-RvD1,RvD5和PGE1显着降低了LPS引发的TNF-α,而TXB2和12-HETE进一步上调了巨噬细胞中LPS增强的IL-6和TNF-α的表达。结论我们的研究结果揭示了抗炎和促炎性脂质体组的同一性,并提出了拔罐治疗的潜在治疗机制。

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