Additional file 1 of Dexamethasone enhances the efficacy of atorvastatin in inhibiting excessively inflammation-induced abnormal angiogenesis by regulating macrophages

Additional file 1: File S1. The inclusion and exclusion criteria. Table S1. RT-PCR Primers used in this study. Table S2. Baseline characteristics and outcome of CSDH patients treated with a combination regimen or ATO monotherapy. Table S3. Baseline characteristics and outcomes of conservatively treated patients who have good efficacy or switched to surgery. Table S4. The functions of these proteins identified, but not specifically discussed in the manuscript. Figure S1. o-ATO and p-ATO in CSDH patients. Figure S2. Concentrations of ATO and DEX in HUVEC. Figure S3. Effects of ATO and DEX on expression of drug transport and catabolism-related proteins in macrophages. Figure S4. Monocytes and macrophages in the haematoma of CSDH patients. Figure S5. The differentiation of THP-1 cells into macrophages stimulated by PMA. Figure S6. LPS can effectively simulate the effect of haematoma on THP-1 macrophages. Figure S7. Regulation of ATO and DEX on the morphological changes of THP-1 macrophages. Figure S8. The effect of ATO and DEX on the MFI of CD86 and CD163 in macrophages. Figure S9. The concentrations of ET-1 in the haematoma, serum and medium supernatant quantified by ELISA.

附加文件1：补充材料S1。本研究的纳入与排除标准。表S1：本研究使用的逆转录聚合酶链反应（RT-PCR）引物。表S2：接受联合治疗方案或三氧化二砷（ATO）单药治疗的慢性硬膜下血肿（CSDH）患者的基线特征与临床转归。表S3：接受保守治疗且疗效良好或后续转为手术治疗的患者的基线特征与临床转归。表S4：本研究已鉴定但未在正文中专门讨论的蛋白质功能。图S1：慢性硬膜下血肿（CSDH）患者体内的o-ATO与p-ATO。图S2：人脐静脉内皮细胞（HUVEC）中三氧化二砷（ATO）与地塞米松（DEX）的浓度。图S3：三氧化二砷（ATO）与地塞米松（DEX）对巨噬细胞药物转运及分解代谢相关蛋白表达的影响。图S4：慢性硬膜下血肿（CSDH）患者血肿内的单核细胞与巨噬细胞。图S5：佛波酯（PMA）诱导THP-1细胞向巨噬细胞分化。图S6：脂多糖（LPS）可有效模拟血肿对THP-1巨噬细胞的作用。图S7：三氧化二砷（ATO）与地塞米松（DEX）对THP-1巨噬细胞形态变化的调控作用。图S8：三氧化二砷（ATO）与地塞米松（DEX）对巨噬细胞CD86、CD163的平均荧光强度（MFI）的影响。图S9：经酶联免疫吸附测定（ELISA）定量检测的血肿、血清及培养基上清液中内皮素-1（ET-1）的浓度。