PROTECTIVE EFFECT OF A PROTEIN KINASE INHIBITOR ON CELLULAR INJURY INDUCED BY CEPHALORIDINE IN THE PORCINE KIDNEY CELL LINE LLC-PK1

  • KAWAI Yoshiko
    Division of Pharmacology, Osaka University of Pharmaceutical Science
  • KOHDA Yuka
    Division of Pharmacology, Osaka University of Pharmaceutical Science
  • GEMBA Munekazu
    Division of Pharmacology, Osaka University of Pharmaceutical Science
  • KODAWARA Takaaki
    Division of Pharmacology, Osaka University of Pharmaceutical Science

書誌事項

公開日
2005
資源種別
journal article
DOI
  • 10.2131/jts.30.157
公開者
一般社団法人 日本毒性学会

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説明

We investigated the effects of a protein kinase C inhibitor and a tyrosine kinase inhibitor on the cellular injury induced by cephaloridine in an established renal epithelial cell line, LLC-PK1. Cephaloridine increased the leakage of lactate dehydrogenase (LDH) from LLC-PK1 cells into the medium and also caused an increase in the level of lipid peroxide (index of oxidative stress) in the cells. Treatment of the cells with a hydroxyl radical scavenger, dimethylthiourea (DMTU), inhibited the increases in LDH leakage and lipid peroxidation in LLC-PK1 cells exposed to cephaloridine. A protein kinase C inhibitor, H-7, and tyrosine kinase inhibitors, genistein and lavendustinA, inhibited the increases in LDH leakage and lipid peroxidation in LLC-PK1 cells exposed to cephaloridine. These results suggest that a signaling pathway which involves protein kinase C and tyrosine kinase plays a role in the generation of reactive oxygen species in LLC-PK1 cells damaged by cephaloridine.<br>

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