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木犀草素、槲皮素、染料木黄酮和槲皮万寿菊素可抑制从H9c2心肌母细胞中获得的脂多糖的作用。

Luteolin, quercetin, genistein and quercetagetin inhibit the effects of lipopolysaccharide obtained from in H9c2 cardiomyoblasts.

作者信息

Gutiérrez-Venegas Gloria, Torras-Ceballos Alfredo, Gómez-Mora Juan Arturo, Fernández-Rojas Berenice

机构信息

Laboratorio de Bioquímica de la División de Estudios de Posgrado de la Facultad de Odontología, Universidad Nacional Autónoma de México Ciudad Universitaria, 04510 México DF, Mexico.

出版信息

Cell Mol Biol Lett. 2017 Sep 4;22:19. doi: 10.1186/s11658-017-0047-z. eCollection 2017.

DOI:10.1186/s11658-017-0047-z
PMID:28878808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5583969/
Abstract

BACKGROUND

One of the microorganisms from dental plaque associated with severe inflammatory responses in infectious endocarditis is . It is a Gram-negative bacteria harvested from chronic periodontitis patients. Lipopolysaccharide (LPS) obtained from promotes the expressions of interleukin-1 (IL-1), IL-6 and tumor necrosis factor alpha (TNF-α). Flavonoids are thought to participate in processes that control inflammation, such as the expression of cyclooxygenase-2 (COX-2).

METHODS

We investigated the effects of luteolin, quercetin, genistein and quercetagetin on cardiomyoblasts treated with LPS alone or in combination with following inhibitors p38 (SB203580), ERK (PD98059), JNK (SP600125) and PKC (Calphostin C) for 1 h. The kinase activation and COX-2 expression levels were determined at the gene and protein levels.

RESULTS

These flavonoids are considered to inhibit the activation of mitogen-activated protein kinase (MAPK) and the degradation of inhibitor of kappa B-alpha (IκB-α). They also play a role in COX-2 expression.

CONCLUSION

We conclude that the tested flavonoids inhibit inflammatory responses induced by LPS in H9c2 cells.

摘要

背景

与感染性心内膜炎严重炎症反应相关的牙菌斑微生物之一是 。它是从慢性牙周炎患者中分离出的革兰氏阴性菌。从 获得的脂多糖(LPS)可促进白细胞介素-1(IL-1)、IL-6和肿瘤坏死因子α(TNF-α)的表达。黄酮类化合物被认为参与控制炎症的过程,如环氧合酶-2(COX-2)的表达。

方法

我们研究了木犀草素、槲皮素、染料木黄酮和芦丁对单独用LPS处理或与以下抑制剂p38(SB203580)、ERK(PD98059)、JNK(SP600125)和PKC(Calphostin C)联合处理1小时的心肌成纤维细胞的影响。在基因和蛋白质水平上测定激酶激活和COX-2表达水平。

结果

这些黄酮类化合物被认为可抑制丝裂原活化蛋白激酶(MAPK)的激活和κB-α抑制剂(IκB-α)的降解。它们在COX-2表达中也起作用。

结论

我们得出结论,所测试的黄酮类化合物可抑制H9c2细胞中LPS诱导的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/f03b921dfe07/11658_2017_47_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/bb748c22d05a/11658_2017_47_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/fbaaac005026/11658_2017_47_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/1b0804bd909e/11658_2017_47_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/8011967cbb11/11658_2017_47_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/956f24319bde/11658_2017_47_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/f03b921dfe07/11658_2017_47_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/bb748c22d05a/11658_2017_47_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/fbaaac005026/11658_2017_47_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/1b0804bd909e/11658_2017_47_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/8011967cbb11/11658_2017_47_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/956f24319bde/11658_2017_47_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8a5/5583969/f03b921dfe07/11658_2017_47_Fig6_HTML.jpg

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