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苄基异硫氰酸酯通过 MAPKs/NF-κB 通路抑制 LPS 刺激的 THP-1 细胞中的炎症小体激活并发挥调节作用。

Benzyl Isothiocyanate Attenuates Inflammasome Activation in LPS-Stimulated THP-1 Cells and Exerts Regulation through the MAPKs/NF-κB Pathway.

机构信息

Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, Korea.

Department of Anesthesiology and Pain Medicine, Busan Paik Hospital, Inje University, Busan 47392, Korea.

出版信息

Int J Mol Sci. 2022 Jan 22;23(3):1228. doi: 10.3390/ijms23031228.

DOI:10.3390/ijms23031228
PMID:35163151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8835927/
Abstract

Inflammasomes are a group of intracellular multiprotein platforms that play important roles in immune systems. Benzyl isothiocyanate (BITC) is a constituent of cruciferous plants and has been confirmed to exhibit various biological activities. The modulatory effects of BITC on inflammasome-mediated interleukin (IL)-1β expression and its regulatory mechanisms in () LPS/ATP-stimulated THP-1 cells was investigated. Monocytic THP-1 cells were treated with phorbol myristate acetate (PMA) to induce differentiation into macrophages. Enzyme-linked immunosorbent assays (ELISA) were performed to measure the levels of IL-1β produced in LPS/ATP-exposed THP-1 cells. Western blotting was performed to examine the BITC modulatory mechanisms in inflammasome-mediated signaling pathways. BITC inhibited IL-1β production in LPS/ATP-induced THP-1 cells. BITC also inhibited activation of leucine-rich repeat protein-3 (NLRP3) and caspase-1 in LPS/ATP-induced THP-1 cells. Furthermore, we show that mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) activation in LPS was attenuated by BITC. These BITC-mediated modulatory effects on IL-1β production may have therapeutic potential for inflammasome-mediated disorders such as a nasal polyp.

摘要

炎性小体是一组在免疫系统中发挥重要作用的细胞内多蛋白平台。苯乙基异硫氰酸酯(BITC)是十字花科植物的成分之一,已被证实具有多种生物活性。本研究旨在探讨 BITC 对 LPS/ATP 刺激的 THP-1 细胞中介炎性小体介导的白细胞介素(IL)-1β表达的调节作用及其调节机制。用佛波醇肉豆蔻酸酯(PMA)处理单核细胞 THP-1 细胞以诱导其分化为巨噬细胞。酶联免疫吸附试验(ELISA)用于测量 LPS/ATP 暴露的 THP-1 细胞中产生的 IL-1β水平。通过 Western blot 检测 BITC 在炎性小体介导的信号通路中的调节机制。BITC 抑制 LPS/ATP 诱导的 THP-1 细胞中 IL-1β的产生。BITC 还抑制了 LPS/ATP 诱导的 THP-1 细胞中富含亮氨酸重复蛋白-3(NLRP3)和半胱天冬酶-1 的激活。此外,我们还表明,BITC 减弱了 LPS 中丝裂原活化蛋白激酶(MAPK)和核因子-κB(NF-κB)的激活。这些 BITC 介导的对 IL-1β产生的调节作用可能对炎性小体介导的疾病(如鼻息肉)具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3794/8835927/ea5bd6c1bfb7/ijms-23-01228-g004.jpg
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