Effects of Capsaicin on Cellular Damage and Monolayer Permeability in Human Intestinal Caco-2 Cells

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  • Tsukura Yuri
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences
  • Mori Maya
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences
  • Hirotani Yoshihiko
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences Laboratory of Clinical Pharmaceutics, Faculty of Pharmacy, Osaka Ohatani University
  • Ikeda Kenji
    Laboratory of Clinical Pharmaceutics, Faculty of Pharmacy, Osaka Ohatani University
  • Amano Fumio
    Laboratory of Biodefense and Regulation, Osaka University of Pharmaceutical Sciences
  • Kato Ryuji
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences
  • Ijiri Yoshio
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences
  • Tanaka Kazuhiko
    Laboratory of Clinical Pharmacy & Clinical Pharmacokinetics, Osaka University of Pharmaceutical Sciences

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Recent studies suggest that capsaicin (Cap), a major constituent of hot pepper, may affect the function and permeability of the intestinal mucosa in vitro. However, the relationships between the dose of Cap and the barrier and/or transporter functions on intestinal epithelial cells are unknown. The aim of this study was to investigate whether Cap initiates cellular injury and alter epithelial permeability in Caco-2 cells. Cellular toxicity, as measured using a lactate dehydrogenase release assay, was not observed at high concentrations of Cap (up to 300 μM). When cell viability was measured by a WST-1 assay (tetrazolium salt-based assay), damage to Caco-2 monolayers was observed at doses of 200 and 300 μM of Cap. The barrier function of tight junctions was assessed by measuring transepithelial electrical resistance (TEER) in Caco-2 cells. Treatment of Caco-2 cells with Cap at doses above 100 μM significantly decreased the TEER compared to treatment with buffer alone for 2 h (p<0.05). We next examined the effects of Cap on the activity of P-glycoprotein (P-gp) found on transcellular transporters. At doses of 100 and 200 μM, Cap inhibited the transport of rhodamine 123 by P-gp-mediated efflux in Caco-2 cells. Cap thus exhibited inhibitory effects on P-gp. The results of this study indicate that Cap, a dietary phytochemical, causes functional and structural changes in Caco-2 cell monolayers at noncytotoxic doses (less than 100 μM of Cap). The concomitant administration of Cap with drugs that are substrates of P-gp might increase the plasma concentrations of such drugs.

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