Effects of the Nonsteroidal Anti-inflammatory Drug Celecoxib on Mitochondrial Function

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  • Tatematsu Yohei
    Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science
  • Fujita Haruhi
    Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science
  • Hayashi Hiroki
    Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science
  • Yamamoto Atsushi
    Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science
  • Tabata Atsushi
    Department of Bioengineering, Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima University
  • Nagamune Hideaki
    Department of Bioengineering, Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima University
  • Ohkura Kazuto
    Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science

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<p>Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to treat inflammation and pain. In the present study, we examined the effects of celecoxib, a cyclooxygenase-2 (COX-2)-selective NSAID, on rat liver mitochondrial function. Celecoxib dose-dependently induced mitochondria swelling, which was not suppressed by cyclosporine A (CsA). The oxygen consumption rate in mitochondria-suspended solution was facilitated by the addition of celecoxib, and its uncoupling activity was observed. Celecoxib also suppressed SF6847-induced uncoupling, and appeared to exert inhibitory effects on the electron transport chain. Celecoxib suppressed the state 3 oxygen consumption rate in the presence of ADP. Protein release from the mitochondrial matrix was detected following the addition of celecoxib, and aldehyde dehydrogenase 2 (ALDH2) and hydroxymethylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2) bands were confirmed in a Western blot analysis. On the other hand, protein release of cytochrome C (CytC), which is an inducer of apoptosis, from the intermembrane space was not observed. Celecoxib enhanced the membrane permeability of human erythrocytes and synthesized liposomes dose-dependently. It then induced the membrane-involving mitochondrial swelling and suppressed mitochondrial function.</p>

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