Effect of inhaled glucocortcoids and their metabolites on CYP3A5 mRNA expression in human lung cells

File 1: Data are peak areas for the metabolites beclomethasone-17-monopropionate ([M1], the active drug) and Δ6-beclomethasone dipropionate ([M5], the CYP3A-mediated metabolite) and the internal standard (IS, prednisolone). Treatment groups were beclomethasone dipropionate (BDP) alone, beclomethasone dipropionate (BDP) plus esterase inhibitors (EI), 1-aminobenzotriazole (1-ABT) plus beclomethasone dipropionate (BDP), and 1-aminobenzotriazole (1-ABT) plus esterase inhibitors (EI) plus the active drug [M1]. Data corresponds to Figure 3A in the main text.
File 2: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups are dimethyl sulfoxide (DMSO, vehicle control), beclomethasone dipropionate (BDP), beclomethasone dipropionate (BDP) plus esterase inhibitors (EI), 1-aminobenzotriazole (1-ABT), 1-aminobenzotriazole (1-ABT) plus beclomethasone dipropionate (BDP), and 1-aminobenzotriazole (1-ABT) plus esterase inhibitors (EI) plus active drug [M1]. Data corresponds to Figure 3B in the main text. 
File 3: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups were dimethyl sulfoxide (DMSO, vehicle control), beclomethasone dipropionate (BDP), ketoconazole (KTZ) at 50 µM plus beclomethasone dipropionate (BDP), ketoconazole (KTZ) at 10 µM plus beclomethasone dipropionate (BDP), and ketoconazole (KTZ) at 1 µM plus beclomethasone dipropionate (BDP). Data corresponds to Figure 4A in the main text. 
File 4: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups were dimethyl sulfoxide (DMSO, vehicle control), budesonide (BUD), ketoconazole (KTZ) at 50 µM plus budesonide (BUD), ketoconazole (KTZ) at 10 µM plus budesonide (BUD), and ketoconazole (KTZ) at 1 µM plus budesonide (BUD). Data corresponds to Figure 4B in the main text.
File 5: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups were dimethyl sulfoxide (DMSO, vehicle control), triamcinolone acetonide (TCL), ketoconazole (KTZ) at 50 µM plus triamcinolone acetonide (TCL), ketoconazole (KTZ) at 10 µM plus triamcinolone acetonide (TCL), and ketoconazole (KTZ) at 1 µM plus triamcinolone acetonide (TCL). Data corresponds to Figure 4C in the main text. 
File 6: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups were dimethyl sulfoxide (DMSO, vehicle control), fluticasone propionate (FLT), ketoconazole (KTZ) at 50 µM plus fluticasone propionate (FLT), ketoconazole (KTZ) at 10 µM plus fluticasone propionate (FLT), and ketoconazole (KTZ) at 1 µM plus fluticasone propionate (FLT). Data corresponds to Figure 4D in the main text.
File 7: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Treatment groups were dimethyl sulfoxide (DMSO, vehicle control), flunisolide (FLN), ketoconazole (KTZ) at 50 µM plus flunisolide (FLN), ketoconazole (KTZ) at 10 µM plus flunisolide (FLN), and ketoconazole (KTZ) at 1 µM plus flunisolide (FLN). Data corresponds to Figure 4E in the main text. 
File 8: Data are copy numbers of CYP3A5*1 mRNA and β-microglobulin (B2M, housekeeping gene) mRNA. Control treatment groups were ketoconazole (KTZ) at 50 µM, ketoconazole (KTZ) at 10 µM, and ketoconazole (KTZ) at 1 µM in the main text.
File 9: Data are represented as copies of mRNA detected for the glucocorticoid receptor (GR) and β-microglobulin (B2M, housekeeping gene) for each treatment group. siRNA directed against the green fluorescent protein (GFP) was used as a negative control and compared to siRNA directed against the glucocorticoid receptor (GR) at 48, 72, and 96 hr post siRNA treatment. Data corresponds to Figure 5A in the main text. 
File 10: Data are copy numbers of mRNA detected for CYP3A5*1 and β-microglobulin (B2M, housekeeping gene). Pretreatments were siRNA directed against either green fluorescent protein (GFP, negative control) or the glucocorticoid receptor (GR). Three treatment groups consisted of dimethyl sulfoxide (DMSO, vehicle control), beclomethasone dipropionate (BDP), and beclomethasone dipropionate (BDP) plus esterase inhibitors (EI). Data corresponds to Figure 5B in the main text. 
File 11: Data are copies of CY3A5*1 mRNA divided by 10,000 copies of β-microglobulin (B2M, housekeeping gene) for each treatment. Treatments were dimethyl sulfoxide (DMSO, vehicle control), beclomethasone dipropionate (BDP), dimethyl sulfoxide (DMSO, vehicle control) treated cells cultured without hydrocortisone (HC), and beclomethasone dipropionate (BDP) treated cells cultured without hydrocortisone (HC). All treatments lasted for 24 hours. Data corresponds to Figure 6 in the main text.

文件1：数据集包含了代谢物倍氯米松-17-单丙酸酯([M1]，活性药物)、Δ6-倍氯米松双丙酸酯([M5]，CYP3A介导的代谢物)以及内标(内标，泼尼松龙)的峰值区域。治疗组包括单独的倍氯米松双丙酸酯(BDP)、倍氯米松双丙酸酯(BDP)加酯酶抑制剂(EI)、1-氨基苯并三唑(1-ABT)加倍氯米松双丙酸酯(BDP)以及1-氨基苯并三唑(1-ABT)加酯酶抑制剂(EI)加活性药物[M1]。数据对应于正文中的图3A。

文件2：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、倍氯米松双丙酸酯(BDP)、倍氯米松双丙酸酯(BDP)加酯酶抑制剂(EI)、1-氨基苯并三唑(1-ABT)、1-氨基苯并三唑(1-ABT)加倍氯米松双丙酸酯(BDP)以及1-氨基苯并三唑(1-ABT)加酯酶抑制剂(EI)加活性药物[M1]。数据对应于正文中的图3B。

文件3：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、倍氯米松双丙酸酯(BDP)、酮康唑(KTZ)在50 µM加倍氯米松双丙酸酯(BDP)、酮康唑(KTZ)在10 µM加倍氯米松双丙酸酯(BDP)以及酮康唑(KTZ)在1 µM加倍氯米松双丙酸酯(BDP)。数据对应于正文中的图4A。

文件4：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、布地奈德(BUD)、酮康唑(KTZ)在50 µM加布地奈德(BUD)、酮康唑(KTZ)在10 µM加布地奈德(BUD)以及酮康唑(KTZ)在1 µM加布地奈德(BUD)。数据对应于正文中的图4B。

文件5：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、曲安奈德(TCL)、酮康唑(KTZ)在50 µM加曲安奈德(TCL)、酮康唑(KTZ)在10 µM加曲安奈德(TCL)以及酮康唑(KTZ)在1 µM加曲安奈德(TCL)。数据对应于正文中的图4C。

文件6：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、氟替卡松丙酸酯(FLT)、酮康唑(KTZ)在50 µM加氟替卡松丙酸酯(FLT)、酮康唑(KTZ)在10 µM加氟替卡松丙酸酯(FLT)以及酮康唑(KTZ)在1 µM加氟替卡松丙酸酯(FLT)。数据对应于正文中的图4D。

文件7：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。治疗组包括二甲基亚砜(DMSO，溶剂对照)、氟尼缩松(FLN)、酮康唑(KTZ)在50 µM加氟尼缩松(FLN)、酮康唑(KTZ)在10 µM加氟尼缩松(FLN)以及酮康唑(KTZ)在1 µM加氟尼缩松(FLN)。数据对应于正文中的图4E。

文件8：数据集为CYP3A5*1 mRNA和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。对照治疗组包括正文中的酮康唑(KTZ)在50 µM、10 µM和1 µM。

文件9：数据集展示了针对每个治疗组的糖皮质激素受体(GR)和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。以针对绿色荧光蛋白(GFP)的siRNA作为阴性对照，并与针对糖皮质激素受体(GR)的siRNA在siRNA处理后48、72和96小时进行比较。数据对应于正文中的图5A。

文件10：数据集为CYP3A5*1和β-微球蛋白(B2M，管家基因) mRNA的拷贝数。预处理包括针对绿色荧光蛋白(GFP，阴性对照)或糖皮质激素受体(GR)的siRNA。三个治疗组包括二甲基亚砜(DMSO，溶剂对照)、倍氯米松双丙酸酯(BDP)以及倍氯米松双丙酸酯(BDP)加酯酶抑制剂(EI)。数据对应于正文中的图5B。

文件11：数据集为每个治疗组的CY3A5*1 mRNA拷贝数除以β-微球蛋白(B2M，管家基因)的10,000个拷贝数。处理包括二甲基亚砜(DMSO，溶剂对照)、倍氯米松双丙酸酯(BDP)、未经氢化可的松(HC)处理的DMSO处理细胞以及未经氢化可的松(HC)处理的倍氯米松双丙酸酯(BDP)处理细胞。所有处理持续24小时。数据对应于正文中的图6。