关键词: atherogenesis atorvastatin gene expression mutagenesis proteomic profile

Mesh : Humans Atorvastatin / pharmacology Endothelial Cells / drug effects metabolism Plasminogen Activator Inhibitor 1 / metabolism genetics Mitomycin / pharmacology Interleukin-8 / metabolism genetics Coronary Vessels / drug effects cytology Anti-Inflammatory Agents / pharmacology Cells, Cultured Macrophage Migration-Inhibitory Factors / genetics metabolism

来  源:   DOI:10.1007/s10517-024-06151-7

Abstract:
The level of cytokine expression was measured in human coronary artery (HCAEC) and internal thoracic artery (HITAEC) endothelial cells exposed to 500 ng/ml alkylating mutagen mitomycin C (MMC) and 5 μM atorvastatin. It was found that treatment of MMC-exposed HCAEC with atorvastatin decreased secretion of macrophage migration inhibitory factor (MIF), IL-8, and IL8 gene expression, but increased the expression of SERPINE1 gene encoding the PAI-1 protein. In atorvastatin-treated HITAEC, the concentration of MIF protein and the expression of the IL8 and SERPINE1 genes were reduced. We can conclude that atorvastatin prevents proinflammatory activation of endothelial cells cultured under conditions of genotoxic load. However, the molecular mechanisms of this effect require further research.
摘要:
在暴露于500ng/ml烷基化诱变剂丝裂霉素C(MMC)和5μM阿托伐他汀的人冠状动脉(HCAEC)和胸廓内动脉(HITAEC)内皮细胞中测量细胞因子表达水平。发现用阿托伐他汀治疗MMC暴露的HCAEC可减少巨噬细胞移动抑制因子(MIF)的分泌,IL-8和IL8基因表达,但增加了编码PAI-1蛋白的SERPINE1基因的表达。在阿托伐他汀治疗的HITAEC中,MIF蛋白浓度降低,IL8和SERPINE1基因表达降低。我们可以得出结论,阿托伐他汀可以防止在基因毒性负荷条件下培养的内皮细胞的促炎激活。然而,这种效应的分子机制需要进一步研究。
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