Molnari Jillissa C, Hassan Hazem E, Myers Alan L
Department of Pharmaceutical, Biomedical and Administrative Sciences, College of Pharmacy and Health Sciences, Drake University, 2507 University Avenue, Des Moines, IA 50266, USA.
Eur J Drug Metab Pharmacokinet. 2012 Mar;37(1):57-63. doi: 10.1007/s13318-011-0065-6. Epub 2011 Sep 17.
Sertraline potently inhibits cytochrome P450 2B6 (CYP2B6) in vitro. Bupropion is commonly co-prescribed with sertraline and is exclusively metabolized by CYP2B6 to its major active metabolite hydroxybupropion. Putatively the co-administration of bupropion and sertraline could lead to a significant pharmacokinetic drug-drug interaction. The aim of this study was to evaluate a possible drug interaction between these drugs in mice. To study this male CF-1 mice were administered sertraline 5 mg/kg once daily for 6 days, followed by a single dose of bupropion 50 mg/kg on the seventh study day. Plasma and brain samples were collected post-bupropion dose for measurement of bupropion and hydroxybupropion levels on HPLC. Pharmacokinetic parameters for bupropion and hydroxybupropion were calculated using noncompartmental analysis and the variance in AUC of each was computed using Bailer's analysis. We found that mice pretreated with sertraline exhibited a small elevation in bupropion metabolism. This was substantiated by Bailer's analysis which indicated that in the presence of sertraline, both plasma and brain bupropion exposure were significantly (p < 0.05) decreased, while plasma hydroxybupropion exposure was significantly (p < 0.05) increased. Also the plasma hydroxybupropion-to-bupropion ratio of AUC was increased by 27% in sertraline treated mice, indicative of increased CYP2B activity. This is the first study, to our knowledge, that reports a mild pharmacokinetic drug-drug interaction between bupropion and sertraline in mice. However, it is unknown whether these quantitative changes in enzyme activity and consequent drug exposure would equate to significant pharmacodynamic changes (e.g., perturbations in brain neurotransmitter levels) observed in the clinic.
舍曲林在体外能有效抑制细胞色素P450 2B6(CYP2B6)。安非他酮通常与舍曲林联合使用,且仅通过CYP2B6代谢为其主要活性代谢产物羟基安非他酮。推测安非他酮与舍曲林的联合使用可能导致显著的药代动力学药物相互作用。本研究的目的是评估这些药物在小鼠体内可能存在的药物相互作用。为研究此问题,雄性CF-1小鼠每天一次给予5 mg/kg舍曲林,持续6天,然后在第7个研究日给予单剂量50 mg/kg安非他酮。在给予安非他酮后采集血浆和脑样本,通过高效液相色谱法测定安非他酮和羟基安非他酮水平。使用非房室分析计算安非他酮和羟基安非他酮的药代动力学参数,并使用贝勒分析计算各自曲线下面积(AUC)的方差。我们发现,用舍曲林预处理的小鼠安非他酮代谢有小幅升高。贝勒分析证实了这一点,该分析表明,在有舍曲林存在的情况下,血浆和脑内安非他酮的暴露量均显著降低(p < 0.05),而血浆中羟基安非他酮的暴露量显著增加(p < 0.05)。此外,在舍曲林处理的小鼠中,AUC的血浆羟基安非他酮与安非他酮比值增加了27%,表明CYP2B活性增强。据我们所知,这是第一项报道安非他酮与舍曲林在小鼠体内存在轻度药代动力学药物相互作用的研究。然而,尚不清楚这些酶活性的定量变化以及随之而来的药物暴露是否等同于临床上观察到的显著药效学变化(例如,脑神经递质水平的扰动)。