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Abstract：
To investigate the mechanism of curcumin (CUR) on vascular calcification (VC), we screen for common targets of CUR and atherosclerosis and verify the targets genes in vivo and in vitro experiments. The common targets of CUR and AS were screened and obtained using different databases. These target genes were analyzed by GO and KEGG pathway enrichment analysis. PPI network analysis was performed and to analyze the key targets. A rat VC model was constructed and CUR was fed for three weeks. The changes of vascular structure and calcium salt deposition were observed in H&E and Von Kossa staining. Further, the expression of these target proteins was detected in the primary VSMCs of VC. The 31 common targets were obtained. GO functional enrichment analysis obtained 1284 terms and KEGG pathway enriched 66 pathways. The key genes were identified in the cytoHubba plugin. The molecular docking analysis showed that CUR bound strongly to EGFR, STAT3 and BCL2. The animal experiments showed the deposition calcium salt reduced by the CUR administration. These proteins BMP2, RUNX2, EGFR, STAT3 and BAX expression were upregulated in VC group and CUR attenuated the upregulated expression. The signal protein Akt and p65 expression increased in VC group and decreased in CUR group. We identified some common target genes of CUR and AS and identified these key genes. The anti-VC effect of CUR was associated with the inhibition of upregulation of EGFR, STAT3 and RUNX2 expression in VSMCs.
摘要：
探讨姜黄素(CUR)对血管钙化(VC)的作用机制。我们筛选了CUR和动脉粥样硬化的共同靶标，并在体内和体外实验中验证了靶基因。使用不同的数据库筛选并获得CUR和AS的共同靶标。通过GO和KEGG途径富集分析来分析这些靶基因。进行PPI网络分析并分析关键目标。建立大鼠VC模型，饲喂CUR3周。在H＆E和VonKossa染色中观察到血管结构和钙盐沉积的变化。Further,在VC的原代VSMC中检测到这些靶蛋白的表达。获得了31个共同目标。GO功能富集分析获得1284条，KEGG途径富集66条。在cytoHubba插件中鉴定了关键基因。分子对接分析显示CUR与EGFR有很强的结合,STAT3和BCL2。动物实验显示通过CUR施用减少了钙盐的沉积。这些蛋白质BMP2，RUNX2，EGFR，VC组STAT3和BAX表达上调，CUR减弱了上调的表达。信号蛋白Akt和p65表达在VC组增加，在CUR组降低。我们确定了CUR和AS的一些常见靶基因，并确定了这些关键基因。CUR的抗VC作用与抑制EGFR的上调有关,STAT3和RUNX2在VSMC中的表达。
