Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
Bull Exp Biol Med. 2024 Jun;177(2):177-180. doi: 10.1007/s10517-024-06151-7. Epub 2024 Aug 2.
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.
在暴露于 500ng/ml 烷化诱变剂丝裂霉素 C (MMC) 和 5μM 阿托伐他汀的人冠状动脉内皮细胞 (HCAEC) 和内乳动脉内皮细胞 (HITAEC) 中测量细胞因子表达水平。结果发现,用阿托伐他汀处理 MMC 暴露的 HCAEC 可降低巨噬细胞迁移抑制因子 (MIF)、IL-8 和 IL8 基因表达的分泌,但增加编码 PAI-1 蛋白的 SERPINE1 基因的表达。在阿托伐他汀处理的 HITAEC 中,MIF 蛋白的浓度和 IL8 和 SERPINE1 基因的表达降低。我们可以得出结论,阿托伐他汀可防止在遗传毒性负荷条件下培养的内皮细胞发生促炎激活。然而,这种作用的分子机制需要进一步研究。