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Lansoprazole inhibits mitochondrial superoxide production and cellular lipid peroxidation induced by indomethacin in RGM1 cells
Authors:Kanho Rai   Hirofumi Matsui   Tsuyoshi Kaneko   Yumiko Nagano   Osamu Shimokawa   Jumpei Udo   Aki Hirayama   Ichinosuke Hyodo   Hiroko P. Indo   Hideyuki J. Majima
Affiliation:1Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan;2The Center of Integrative Medicine, Tsukuba University of Technology, 4-12-7 Kasuga, Tsukuba, Ibaraki 305-8575, Japan;3The Department of Oncology and Department of Space Environmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan
Abstract:Lansoprazole is effective in healing non-steroidal anti-inflammatory drugs induced ulcers, and antioxidant properties have been thought to play a key role in healing ulcers. We hypothesize that lansoprazole exerts a cytoprotective effect by inhibiting reactive oxygen species leakage from mitochondria and lipid peroxidation. We pretreated gastric epithelial RGM1 cells with lansoprazole and then treated them with indomethacin in vitro. We found that the lansoprazole pretreatment significantly reduced cellular injury, maintained mitochondrial transmembrane potential, and decreased lipid peroxidation. Furthermore, the signal intensity of the electron spin resonance spectrum of the indomethacin-treated mitochondria which were pretreated with lansoprazole showed considerable reduction compared to those without the lansoprazole pretreatment. These results suggest that lansoprazole reduced superoxide production in the mitochondria of indomethacin treated cells, and subsequently inhibited lipid peroxide and cellular injury in gastric epithelial cells.
Keywords:lansoprazole   superoxide   lipid peroxidation   electron spin resonance   indomethacin
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