Isoliquiritigenin pretreatment attenuates cisplatin induced proximal tubular cells (LLC-PK1) death and enhances the toxicity induced by this drug in bladder cancer T24 cell line

被引:25
作者
Patricia Moreno-Londono, Angela [1 ]
Bello-Alvarez, Claudia [1 ]
Pedraza-Chaverri, Jose [1 ]
机构
[1] Natl Autonomous Univ Mexico UNAM, Fac Chem, Dept Biol, Mexico City 04510, DF, Mexico
关键词
Cisplatin; Isoliquiritigenin; Nephrotoxicity; Heme oxygenase-1; Antioxidants; HEME OXYGENASE-1 GENE; NF-KAPPA-B; OXIDATIVE STRESS; INDUCED APOPTOSIS; CARBON-MONOXIDE; NF-E2-RELATED FACTOR-2; INDUCED NEPHROTOXICITY; NUCLEAR TRANSLOCATION; PROTECTIVE ROLE; MOLECULAR-BASIS;
D O I
10.1016/j.fct.2017.08.047
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Cisplatin is an effective antineoplastic agent widely used in the treatment of solid tumors, however, it induces nephrotoxicity. Cisplatin-induced nephrotoxicity is associated with increased reactive oxygen species (ROS) production and decreased antioxidant system defense in kidney. Isoliquiritigenin (IsoLQ) is a chalcone, which is characterized by its antioxidant and antiinflammatory properties. Herein, we investigated the protective effect of IsoLQ on LLC-PK1 proximal tubular cells against cisplatin-induced death and its effect on the antineoplastic activity of cisplatin on bladder cancer T24 cell line. It was found that pretreatment with IsoLQ attenuates cisplatin-induced cell death, ROS production, and activation of caspase-3. IsoLQ also induced heme oxygenase-1 (HO-1) expression that may be associated with nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation. The protective effect of IsoLQ was abrogated by tin mesoporphyrin (SnMP), an HO inhibitor. Further, bilirubin and carbon monoxide releasing molecule-2 also showed a protective effect against cisplatin-induced cell death. In addition, IsoLQ induced in a dose-dependent way, death of T24 cells and exacerbated cisplatin-induced cell death. These results suggest that IsoLQ has a protective effect on cisplatin-induced toxicity in LLC-PK1 cells, in part through induction of HO-1, without interfering with the antineoplastic activity of this agent in T24 cells. (C) 2017 Published by Elsevier Ltd.
引用
收藏
页码:143 / 154
页数:12
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