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The effect of sinomenine on ERK1/2, JNK and p38 phosphorylation in LPS-stimulated endothelial cells.

文献类型： 外文期刊

作者： Yang, Haifeng 1 ; Chen, Xiaolan 1 ; Li, Yanyan 1 ; Wang, Jing 1 ; Shi, Feifei 1 ; Li, Bin 2 ; Hu, Yiyi 2 ;

作者机构： 1.Jiangsu Agri Anim Husb Vocat Coll, 8 East Phoenix Rd, Taizhou 225300, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Vet Med, Jiangsu Key Lab Food Qual & Safety, State Key Lab Cultivat Base,Minist Sci & Technol, 50 Zhong ling St, Nanjing 210014, Peoples R China

3.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Peoples R China

关键词： inflammation; endocrine; signal pathway; phosphorylation; alkaloid

期刊名称：NEUROENDOCRINOLOGY LETTERS （ 影响因子：0.7； 五年影响因子：0.9 ）

ISSN： 0172-780X

年卷期： 2023 年 44 卷 1 期

页码：

收录情况： SCI

摘要： This study was to investigate the effect of sinomenine by LPS-induced MAPK phosphorylation in endothelial cells. Endothelial cells were challenged with different doses LPS and/or treated with sinomenine at three concentrations (1, 5, or 10 mu g/mL) in pathological model, drug safety, treatment and prevention experiments. The cells were incubated at 37 degrees C in a cell incubator total for 24 h. The lysate cells were collected and analyzed the phosphorylation of ERK1/2, JNK and p38 by MAPK phosphoprotein assay whole cell lysate kit. As expected, LPS could significantly elevated phosphorylation of ERK1/2, JNK and p38, but sinomenine not. The results revealed that sinomenine significantly reduced the phosphorylation of ERK1/2 and p38 in treatment experiment, and inhibited phosphorylation of ERK1/2, JNK and p38 in prevention experiment. Our findings demonstrated that sinomenine protects endothelial cells from LPS-induced inflammation, which might be associated with depressing MAPK signaling pathway.

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