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木犀草素-3'-磷酸通过调控 RAW 264.7 细胞中的 NF-κB/MAPK 级联信号通路抑制脂多糖诱导的炎症反应。

Luteolin-3'--Phosphate Inhibits Lipopolysaccharide-Induced Inflammatory Responses by Regulating NF-κB/MAPK Cascade Signaling in RAW 264.7 Cells.

机构信息

Department of Pharmaceutical Engineering & Biotechnology, Sunmoon University, Asan 31460, Korea.

Natural Product Informatics Research Center, Korea Institute of Science and Technology (KIST), Gangneung 25451, Korea.

出版信息

Molecules. 2021 Dec 6;26(23):7393. doi: 10.3390/molecules26237393.

Abstract

Luteolin (LT), present in most plants, has potent anti-inflammatory properties both in vitro and in vivo. Furthermore, some of its derivatives, such as luteolin-7--glucoside, also exhibit anti-inflammatory activity. However, the molecular mechanisms underlying luteolin-3'--phosphate (LTP)-mediated immune regulation are not fully understood. In this paper, we compared the anti-inflammatory properties of LT and LTP and analyzed their molecular mechanisms of action; we obtained LTP via the biorenovation of LT. We investigated the anti-inflammatory activities of LT and LTP in macrophage RAW 264.7 cells. We confirmed from previously reported literature that LT inhibits the production of nitric oxide and prostaglandin E, as well as the expression of inducible NO synthetase and cyclooxygenase-2. In addition, expressions of inflammatory genes and mediators, such as tumor necrosis factor-α, interleukin-6, and interleukin-1β, were suppressed. LTP showed anti-inflammatory activity similar to LT, but better anti-inflammatory activity in all the experiments, while also inhibiting mitogen-activated protein kinase and nuclear factor-kappa B more effectively than LT. At a concentration of 10 μM, LTP showed differences of 2.1 to 44.5% in the activity compared to LT; it also showed higher anti-inflammatory activity. Our findings suggest that LTP has stronger anti-inflammatory activity than LT.

摘要

木樨草素(LT)存在于大多数植物中,具有体外和体内的强大抗炎特性。此外,其一些衍生物,如木樨草素-7-O-葡萄糖苷,也具有抗炎活性。然而,木樨草素-3'-磷酸(LTP)介导的免疫调节的分子机制尚不完全清楚。在本文中,我们比较了 LT 和 LTP 的抗炎特性,并分析了它们的作用机制;我们通过 LT 的生物转化获得了 LTP。我们研究了 LT 和 LTP 在巨噬细胞 RAW 264.7 细胞中的抗炎活性。我们从之前的文献报道中证实,LT 抑制一氧化氮和前列腺素 E 的产生,以及诱导型一氧化氮合酶和环氧化酶-2 的表达。此外,炎症基因和介质的表达,如肿瘤坏死因子-α、白细胞介素-6 和白细胞介素-1β,也受到抑制。LTP 表现出与 LT 相似的抗炎活性,但在所有实验中表现出更好的抗炎活性,同时也比 LT 更有效地抑制丝裂原激活蛋白激酶和核因子-κB。在 10 μM 浓度下,LTP 的活性与 LT 相比差异为 2.1%至 44.5%;它也表现出更高的抗炎活性。我们的研究结果表明,LTP 比 LT 具有更强的抗炎活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/693a/8659157/8ce4c988dff8/molecules-26-07393-g001.jpg

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