Imaoka Ayuko, Hattori Tomoki, Akiyoshi Takeshi, Ohtani Hisakazu
Division of Clinical Pharmacokinetics, Keio University Faculty of Pharmacy, Tokyo, Japan.
Department of Clinical Pharmacy, School of Medicine, Keio University, Tokyo, Japan.
Biopharm Drug Dispos. 2023 Oct;44(5):372-379. doi: 10.1002/bdd.2372. Epub 2023 Jul 28.
Irinotecan causes severe gastrointestinal damage, which may affect the expression of intestinal transporters. However, neither the expression of peptide transporter 1 (Pept1) nor the pharmacokinetics of Pept1 substrate drugs has been investigated under irinotecan-induced gastrointestinal damage. Therefore, the present study quantitatively investigated the effects of irinotecan-induced gastrointestinal damage on the intestinal expression of Pept1 and absorption of cephalexin (CEX), a typical Pept1 substrate, in rats. Irinotecan was administered intravenously to rats for 4 days to induce gastrointestinal damage. The expression of Pept1 mRNA and the Pept1 protein in the upper, middle, and lower segments of the small intestine of irinotecan-treated rats was assessed by quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. The pharmacokinetic profile of CEX was examined after its oral or intravenous administration (10 mg/kg). In irinotecan-treated rats, ∼2-fold increases in Pept1 protein levels were observed in all three segments, whereas mRNA levels remained unchanged. The oral bioavailability of CEX significantly decreased to 76% of that in control rats. The decrease in passive diffusion caused by intestinal damage may have overcome the increase in Pept1-mediated uptake. In conclusion, irinotecan may decrease the intestinal absorption of Pept1 substrate drugs; however, it increased the expression of intestinal Pept1.
伊立替康会导致严重的胃肠道损伤,这可能会影响肠道转运体的表达。然而,在伊立替康诱导的胃肠道损伤情况下,肽转运体1(Pept1)的表达以及Pept1底物药物的药代动力学均未得到研究。因此,本研究定量考察了伊立替康诱导的胃肠道损伤对大鼠肠道Pept1表达及典型Pept1底物头孢氨苄(CEX)吸收的影响。给大鼠静脉注射伊立替康4天以诱导胃肠道损伤。分别通过定量实时聚合酶链反应(PCR)和蛋白质免疫印迹法评估伊立替康处理大鼠小肠上段、中段和下段中Pept1 mRNA和Pept1蛋白的表达。口服或静脉注射(10 mg/kg)CEX后检测其药代动力学特征。在伊立替康处理的大鼠中,所有三个肠段的Pept1蛋白水平均观察到约2倍的升高,而mRNA水平保持不变。CEX的口服生物利用度显著降低至对照大鼠的76%。肠道损伤引起的被动扩散减少可能抵消了Pept1介导的摄取增加。总之,伊立替康可能会降低Pept1底物药物的肠道吸收;然而,它增加了肠道Pept1的表达。