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总黄酮通过抑制 TLR2 介导的 NF-κB 和 MAPK 通路缓解脂多糖诱导的肺损伤。

Total Flavonoids from Alleviated -Induced Lung Injury via Inhibition of the TLR2-Mediated NF-κB and MAPK Pathways.

机构信息

Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang 421001, China.

Research Lab of Translational Medicine, Hengyang Medical College, University of South China, Hengyang 421001, China.

出版信息

Molecules. 2023 Oct 13;28(20):7077. doi: 10.3390/molecules28207077.

DOI:10.3390/molecules28207077
PMID:37894556
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10609408/
Abstract

() is an atypical bacterial pathogen responsible for community-acquired pneumonia primarily among school-aged children and young adults. () has been used as a medicinal and edible plant in China for centuries, the constituents from which possessed various bioactivities. Notably, flavonoids existing in residues of defatted seeds exhibited significant anti-inflammatory activities. In the present study, we investigated the impact of total flavonoids from (TFCO) seed extract on pneumonia. TFCO was obtained using multiple column chromatography methods and identified as kaempferol glycosides via UPLC-HRESIMS. In a pneumonia mouse model, TFCO significantly reduced the lung damage, suppressed IL-1β, IL-6, and TNF-α production, and curbed TLR2 activation triggered by . Similarly, in RAW264.7 macrophage cells stimulated by lipid-associated membrane proteins (LAMPs), TFCO suppressed the generation of proinflammatory cytokines and TLR2 expression. Moreover, TFCO diminished the phosphorylation of IκBα, JNK, ERK, p38, and p65 nuclear translocation in vitro. In conclusion, TFCO alleviated -induced lung damage via inhibition of TLR2-mediated NF-κB and MAPK pathways, suggesting its potential therapeutic application in -triggered lung inflammation.

摘要

()是一种非典型的细菌病原体,主要引起学龄儿童和青年社区获得性肺炎。()在中国已被用作药用和食用植物数百年,其成分具有多种生物活性。值得注意的是,存在于脱脂种子残渣中的类黄酮表现出显著的抗炎活性。在本研究中,我们研究了()种子提取物总黄酮(TFCO)对肺炎的影响。TFCO 是通过多种柱层析方法获得的,并通过 UPLC-HRESIMS 鉴定为山奈酚糖苷。在肺炎小鼠模型中,TFCO 显著减轻了肺损伤,抑制了白细胞介素 1β(IL-1β)、白细胞介素 6(IL-6)和肿瘤坏死因子-α(TNF-α)的产生,并抑制了由脂膜蛋白(LAMPs)刺激的 RAW264.7 巨噬细胞中 TLR2 的激活。此外,TFCO 抑制了体外促炎细胞因子和 TLR2 的表达。此外,TFCO 减少了 IκBα、JNK、ERK、p38 和 p65 核易位的磷酸化。总之,TFCO 通过抑制 TLR2 介导的 NF-κB 和 MAPK 通路缓解诱导的肺损伤,表明其在诱导的肺炎症中的潜在治疗应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/e437a7f1f014/molecules-28-07077-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/6184a397c541/molecules-28-07077-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/df3ddf091838/molecules-28-07077-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/e347b3b85e70/molecules-28-07077-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/bd3cf7f8882b/molecules-28-07077-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/3374d9a1bf53/molecules-28-07077-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/d3de448f2ff7/molecules-28-07077-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/e437a7f1f014/molecules-28-07077-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/6184a397c541/molecules-28-07077-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/df3ddf091838/molecules-28-07077-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/e347b3b85e70/molecules-28-07077-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/bd3cf7f8882b/molecules-28-07077-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/3374d9a1bf53/molecules-28-07077-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/d3de448f2ff7/molecules-28-07077-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a12b/10609408/e437a7f1f014/molecules-28-07077-g007.jpg

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