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首页> 外文期刊>Cell biology international. >Notch receptor expression in Trypanosoma cruzi Trypanosoma cruzi ‐infected human umbilical vein endothelial cells treated with benznidazole or simvastatin revealed by microarray analysis
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Notch receptor expression in Trypanosoma cruzi Trypanosoma cruzi ‐infected human umbilical vein endothelial cells treated with benznidazole or simvastatin revealed by microarray analysis

机译：在胰蛋白酶瘤Cruzi TrypanoSoma Cruzi-infacted人脐静脉内皮细胞的缺口受体表达，用苯并咪唑或辛伐他汀揭示的微阵列分析

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摘要

Abstract Chagas disease is a vector‐borne disease caused by the protozoan parasite Trypanosoma cruzi . Current therapy involves benznidazole. Benznidazole and other drugs can modify gene expression patterns, improving the response to the inflammatory influx induced by T. cruzi and decreasing the endothelial activation or immune cell recruitment, among other effects. Here, we performed a microarray analysis of human umbilical vein endothelial cells (HUVECs) treated with benznidazole and the anti‐inflammatory drugs acetylsalicylic acid or simvastatin and infected with T. cruzi . Parasitic infection produces differential expression of a set of genes in HUVECs treated with benznidazole alone or a combination with simvastatin or acetylsalicylic acid. The differentially expressed genes were involved in inflammation, adhesion, cardiac function, and remodeling. Notch1 and high mobility group B1 were genes of interest in this analysis due to their importance in placental development, cardiac development, and inflammation. Quantitative polymerase chain reaction confirmation of these two genes indicated that both are upregulated in the presence of benznidazole.
机译：摘要查加斯病是一种由原生动物寄生虫克鲁兹锥虫引起的媒介传播疾病。目前的治疗包括苯硝唑。苯硝唑和其他药物可以改变基因表达模式，改善对T.cruzi诱导的炎症内流的反应，减少内皮细胞活化或免疫细胞募集，以及其他作用。在这里，我们对苯硝唑和抗炎药乙酰水杨酸或辛伐他汀治疗并感染克鲁兹锥虫的人脐静脉内皮细胞（HUVEC）进行了微阵列分析。寄生虫感染在单用苯硝唑或与辛伐他汀或乙酰水杨酸联合治疗的HUVEC中产生一组基因的差异表达。这些差异表达的基因与炎症、粘附、心功能和重塑有关。Notch1和高迁移率族B1是本次分析中感兴趣的基因，因为它们在胎盘发育、心脏发育和炎症中具有重要意义。定量聚合酶链反应对这两个基因的确认表明，在苯硝唑的存在下，这两个基因都上调。

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