青藤碱对lps刺激内皮细胞ERK1/2、JNK和p38磷酸化的影响。

Pub Date : 2023-03-08
Haifeng Yang, Xiaolan Chen, Yanyan Li, Jing Wang, Feifei Shi, Bin Li, Yiyi Hu
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引用次数: 0

摘要

本研究旨在探讨青藤碱通过lps诱导内皮细胞MAPK磷酸化的作用。采用不同剂量LPS刺激内皮细胞和青藤碱(1、5、10 μg/mL)处理内皮细胞进行病理模型、药物安全性、治疗和预防实验。将细胞在37℃的细胞培养箱中孵育24 h,收集裂解细胞,使用MAPK磷酸化蛋白测定全细胞裂解试剂盒分析ERK1/2、JNK和p38的磷酸化水平。正如预期的那样,LPS可以显著提高ERK1/2、JNK和p38的磷酸化,而青藤碱则没有。结果显示青藤碱在治疗组显著降低ERK1/2和p38的磷酸化水平,在预防组显著抑制ERK1/2、JNK和p38的磷酸化水平。我们的研究结果表明青藤碱可以保护内皮细胞免受lps诱导的炎症,这可能与抑制MAPK信号通路有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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The effect of sinomenine on ERK1/2, JNK and p38 phosphorylation in LPS-stimulated endothelial cells.

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 μg/mL) in pathological model, drug safety, treatment and prevention experiments. The cells were incubated at 37 °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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