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首页> 外文期刊>Cell biology international. >Mycophenolic acid regulates spleen tyrosine kinase to repress tumour necrosis factor-alpha-induced monocyte chemotatic protein-1 production in cultured human aortic endothelial cells.
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Mycophenolic acid regulates spleen tyrosine kinase to repress tumour necrosis factor-alpha-induced monocyte chemotatic protein-1 production in cultured human aortic endothelial cells.

机译：霉酚酸调节脾酪氨酸激酶，以抑制培养的人主动脉内皮细胞中肿瘤坏死因子-α诱导的单核细胞趋化蛋白1的产生。

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摘要

Atherosclerosis develops from cascades of inflammatory processes. Spleen tyrosine kinase (Syk) and monocyte chemotatic protein-1 (MCP-1) play important roles in the pathogenesis of atherosclerosis. Mycophenolic acid (MPA) has an anti-inflammatory effect. We have investigated whether MPA regulates Syk to repress tumour necrosis factor-α (TNF-α)-induced MCP-1 production in cultured human aortic endothelial cells. Expression of MCP-1 mRNA and its protein were measured by real time RT-PCR and ELISA, respectively. Reactive oxygen species (ROS) production were measured using 2'7'-dichlorofluorescein diacetate. Activation of AP-1 and NF-κB were assessed by electrophoretic mobility shift assay. Tyrosine phosphorylation of Syk was examined by Western blot analysis. TNF-α increased MCP-1 at both mRNA and protein levels. TNF-α-induced MCP-1 mRNA expression was inhibited by N-acetylcysteine (NAC), Syk inhibitor, Syk-siRNA and MPA. TNF-α-induced MCP-1 protein production was also inhibited by Syk inhibitor and MPA. TNF-α increased DNA binding activity of AP-1 and NF-κB, whereas both AP-1 and NF-κB decoy oligodeoxynucleotides downregulated TNF-α-induced MCP-1 mRNA expression. TNF-α increased ROS generation, which was inhibited by NAC and MPA, but not by Syk inhibitor. TNF-α increased tyrosine phosphorylation of Syk, which was attenuated by NAC and MPA. MPA and Syk inhibitor attenuated TNF-α-induced DNA binding activity of NF-κB and AP-1. TNF-α induced MCP-1 expression via activation of AP-1 and NF-κB. AP-1 and NF-κB were mediated through ROS, followed by Syk. MPA exerts anti-inflammatory effect by inhibiting MCP-1 expression via suppression of ROS and Syk.
机译：动脉粥样硬化从炎症过程的级联发展而来。脾酪氨酸激酶（Syk）和单核细胞趋化蛋白1（MCP-1）在动脉粥样硬化的发病机理中起重要作用。麦考酚酸（MPA）具有抗炎作用。我们已经研究了MPA是否调节Syk来抑制培养的人主动脉内皮细胞中的肿瘤坏死因子-α（TNF-α）诱导的MCP-1产生。通过实时RT-PCR和ELISA分别测量MCP-1 mRNA及其蛋白的表达。使用2'7'-二氯荧光素二乙酸酯测量活性氧（ROS）的产生。通过电泳迁移率变动分析评估AP-1和NF-κB的激活。通过蛋白质印迹分析检查了Syk的酪氨酸磷酸化。 TNF-α在mRNA和蛋白质水平上均增加MCP-1。 N-乙酰半胱氨酸（NAC），Syk抑制剂，Syk-siRNA和MPA抑制TNF-α诱导的MCP-1 mRNA表达。 Syk抑制剂和MPA也抑制了TNF-α诱导的MCP-1蛋白的产生。 TNF-α增加了AP-1和NF-κB的DNA结合活性，而AP-1和NF-κB诱饵寡聚脱氧核苷酸均下调了TNF-α诱导的MCP-1 mRNA表达。 TNF-α增加了ROS的生成，这被NAC和MPA抑制，但未被Syk抑制剂抑制。 TNF-α增强了Syk的酪氨酸磷酸化，这被NAC和MPA减弱。 MPA和Syk抑制剂减弱了TNF-α诱导的NF-κB和AP-1的DNA结合活性。 TNF-α通过激活AP-1和NF-κB诱导MCP-1表达。 AP-1和NF-κB通过ROS介导，随后是Syk。 MPA通过抑制ROS和Syk抑制MCP-1表达来发挥抗炎作用。

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