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-kaur-15-烯-17-酸-18-醛对脂多糖刺激的 RAW264.7 细胞的抗炎作用与 NF-κB 和 P38/MAPK 通路有关。

The anti-inflammatory effect of -kaur-15-en-17-al-18-oic acid on lipopolysaccharide-stimulated RAW264.7 cells associated with NF-κB and P38/MAPK pathways.

机构信息

Marine College, Shandong University, Weihai 264209, China.

School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China.

出版信息

J Asian Nat Prod Res. 2021 Jun;23(6):570-583. doi: 10.1080/10286020.2020.1786371. Epub 2020 Jun 30.

Abstract

-kaur-15-en-17-al-18-oic acid (LL-3) was demonstrated that it can inhibit LPS-induced nitric oxide (NO) production and macrophage migration, maintain homeostasis of oxidative stress, including increased mitochondrial membrane potential (MMP), decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and maintenance of superoxide dismutase (SOD) and glutathione (GSH) activities and inhibit oxidative stress-induced P38 and nuclear factor κB (NF-κB) pathways to decrease inducible nitric oxide synthase (iNOS), cyclooxygense-2 (COX-2), and tumour necrosis factor (TNF)-α mRNA expressions without marked cytotoxicity. These findings revealed that LL-3 could serve as a candidate lead compound for further studying anti-inflammatory therapies.[Formula: see text].

摘要

-kaur-15-en-17-al-18-oic acid (LL-3) 被证明可以抑制 LPS 诱导的一氧化氮 (NO) 产生和巨噬细胞迁移,维持氧化应激的动态平衡,包括增加线粒体膜电位 (MMP)、降低活性氧 (ROS) 和丙二醛 (MDA) 的水平,维持超氧化物歧化酶 (SOD) 和谷胱甘肽 (GSH) 的活性,并抑制氧化应激诱导的 P38 和核因子 κB (NF-κB) 途径,降低诱导型一氧化氮合酶 (iNOS)、环氧化酶-2 (COX-2) 和肿瘤坏死因子 (TNF)-α mRNA 的表达,而没有明显的细胞毒性。这些发现表明,LL-3 可以作为进一步研究抗炎治疗的候选先导化合物。[公式:见正文]。

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