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来自 的叶绿醇可防止巨噬细胞极化过程中NF-κB介导的炎症反应。

Phytol from prevents NF-κB-mediated inflammatory responses during macrophage polarization.

作者信息

Duraisamy Parimalanandhini, Angusamy Annapoorani, Ravi Sangeetha, Krishnan Mahalakshmi, Martin Livya Catherene, Manikandan Beulaja, Sundaram Janarthanan, Ramar Manikandan

机构信息

Department of Zoology, University of Madras, Guindy Campus, Chennai, 600025 India.

Department of Biochemistry, Annai Veilankanni's College for Women, Chennai, 600015 India.

出版信息

3 Biotech. 2024 Mar;14(3):80. doi: 10.1007/s13205-024-03924-9. Epub 2024 Feb 17.

DOI:10.1007/s13205-024-03924-9
PMID:38375513
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10874368/
Abstract

UNLABELLED

Macrophages are primary immune cells that mediate a wide range of inflammatory diseases through their polarization potential. In this study, phytol isolated from has been explored against 7-ketocholesterol and bacterial lipopolysaccharide-induced macrophage polarization in IC-21 cells. Isolated phytol has been characterized using GC-MS, TLC, HPTLC, FTIR, H-NMR, and HPLC analyses. The immunomodulatory effects of viable concentrations of phytol were tested on oxidative stress, arginase activity, nuclear and mitochondrial membrane potentials in IC-21 cells in addition to the modulation of calcium and lipids. Further, gene and protein expression of atherogenic markers were studied. Results showed that the isolated phytol at a viable concentration of 400 µg/ml effectively reduced the production of nitric oxide, superoxide anion (ROS generation), calcium and lipid accumulation, stabilized nuclear and mitochondrial membranes, and increased arginase activity. The atherogenic markers including iNOS, COX-2, IL-6, IL-1β, MMP-9, CD36, and NF-κB were significantly downregulated at the levels of gene and protein expression, while macrophage surface and nuclear receptor markers (CD206, CD163, and PPAR-γ) were significantly upregulated by phytol pre-treatment in macrophages. Therefore, the present pharmacognostic study supports the role of phytol isolated from in preventing M2-M1 macrophage polarization under inflammatory conditions, making it a promising compound.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s13205-024-03924-9.

摘要

未标记

巨噬细胞是主要的免疫细胞,通过其极化潜能介导多种炎症性疾病。在本研究中,已对从[具体来源未提及]分离出的叶绿醇针对7-酮胆固醇和细菌脂多糖诱导的IC-21细胞中巨噬细胞极化的作用进行了探索。已使用气相色谱-质谱联用(GC-MS)、薄层色谱(TLC)、高效薄层色谱(HPTLC)、傅里叶变换红外光谱(FTIR)、氢核磁共振(H-NMR)和高效液相色谱(HPLC)分析对分离出的叶绿醇进行了表征。除了对钙和脂质的调节外,还测试了叶绿醇活性浓度对IC-21细胞氧化应激、精氨酸酶活性、核膜和线粒体膜电位的免疫调节作用。此外,还研究了致动脉粥样硬化标志物的基因和蛋白表达。结果表明,活性浓度为400μg/ml的分离叶绿醇有效降低了一氧化氮、超氧阴离子(ROS生成)、钙和脂质的积累,稳定了核膜和线粒体膜,并提高了精氨酸酶活性。包括诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、基质金属蛋白酶-9(MMP-9)、CD36和核因子κB(NF-κB)在内的致动脉粥样硬化标志物在基因和蛋白表达水平上显著下调,而巨噬细胞表面和核受体标志物(CD206、CD163和过氧化物酶体增殖物激活受体γ(PPAR-γ))在巨噬细胞中经叶绿醇预处理后显著上调。因此,本生药学研究支持从[具体来源未提及]分离出的叶绿醇在炎症条件下预防M2-M1巨噬细胞极化中的作用,使其成为一种有前景的化合物。

补充信息

在线版本包含可在10.1007/s13205-024-03924-9获取的补充材料。

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