Department of Pharmaceutical Sciences, School of Pharmacy, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Drug Metab Dispos. 2010 Jan;38(1):157-67. doi: 10.1124/dmd.109.029199.
Although oxycodone is the most often used opioid agonist, it remains one of the most understudied drugs. We used microarray analysis to better understand the global changes in gene expression in brain tissues of rats repeatedly treated with oxycodone. Many genes were significantly regulated by oxycodone (e.g., Fkbp5, Per2, Rt1.Dalpha, Slc16a1, and Abcg2). Validation of the microarray data by quantitative real-time-polymerase chain reaction (Q-PCR) indicated that there was a strong significant correlation (r = 0.979, p < 0.0000001) between the Q-PCR and the microarray data. Using MetaCore (a computational platform), many biological processes were identified [e.g., organic anion transport (p = 7.251 x 10(-4)) and regulation of immune response (p = 5.090 x 10(-4))]. Among the regulated genes, Abcg2 mRNA was up-regulated by 2.1-fold, which was further confirmed by immunoblotting (1.8-fold up-regulation). Testing the Abcg2 affinity status of oxycodone using an Abcg2 ATPase assay suggests that oxycodone behaves as an Abcg2 substrate only at higher concentrations (> or = 500 microM). Furthermore, brain uptake studies demonstrated that oxycodone-induced Abcg2 up-regulation resulted in a significant (p < 0.05) decrease (approximately 2-fold) in brain/plasma ratios of mitoxantrone. These results highlight markers/mediators of neuronal responses and identify regulatory pathways involved in the pharmacological action of oxycodone. These results also identify genes that potentially modulate tolerance, dependence, immune response, and drug-drug interactions. Finally, our findings suggest that oxycodone-induced up-regulation of Abcg2 enhanced the efflux of the Abcg2 substrate, mitoxantrone, limiting its brain accumulation and resulting in an undesirable drug-drug interaction. Extrapolating these results to other Abcg2 substrates (e.g., daunorubicin and doxorubicin) indicates that the brain uptake of these agents may be affected if they are administered concomitantly with oxycodone.
虽然羟考酮是最常使用的阿片类激动剂,但它仍然是研究最少的药物之一。我们使用微阵列分析来更好地了解反复接受羟考酮治疗的大鼠脑组织中基因表达的全局变化。许多基因被羟考酮显著调控(例如,Fkbp5、Per2、Rt1.Dalpha、Slc16a1 和 Abcg2)。通过定量实时聚合酶链反应(Q-PCR)对微阵列数据进行验证表明,Q-PCR 和微阵列数据之间存在很强的显著相关性(r = 0.979,p < 0.0000001)。使用 MetaCore(一个计算平台),确定了许多生物学过程[例如,有机阴离子转运(p = 7.251 x 10(-4)) 和免疫反应调节(p = 5.090 x 10(-4))]。在受调控的基因中,Abcg2 mRNA 上调了 2.1 倍,免疫印迹进一步证实了这一点(上调 1.8 倍)。使用 Abcg2 ATP 酶测定法测试羟考酮对 Abcg2 亲和力的状态表明,羟考酮仅在较高浓度(>或= 500 microM)下表现为 Abcg2 底物。此外,脑摄取研究表明,羟考酮诱导的 Abcg2 上调导致米托蒽醌的脑/血浆比率显著(p < 0.05)降低(约 2 倍)。这些结果突出了神经元反应的标志物/介质,并确定了参与羟考酮药理学作用的调节途径。这些结果还确定了可能调节耐受、依赖、免疫反应和药物相互作用的基因。最后,我们的发现表明,羟考酮诱导的 Abcg2 上调增强了 Abcg2 底物米托蒽醌的外排,限制了其在大脑中的积累,并导致不理想的药物相互作用。将这些结果推断到其他 Abcg2 底物(例如,柔红霉素和阿霉素)表明,如果同时给予羟考酮,这些药物的脑摄取可能会受到影响。