| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5846630 | Toxicology and Applied Pharmacology | 2013 | 9 Pages |
Abstract
⺠5-AIQ, a PARP inhibitor, decreased H2O2-induced H9c2 cell death and apoptosis. ⺠5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ⺠5-AIQ decreased H2O2-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ⺠5-AIQ activated Akt and GSK-3β, the effect being abolished by PI3K inhibitor LY294002. ⺠LY294002 attenuated 5-AIQ-mediated effects on H9c2 apoptosis and related proteins.
Keywords
PBS3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromideERKCATFBSJnkDMEMc-Jun N-terminal protein kinaseDMSOMAPKsMTTROSMyocardial apoptosissodium dodecyl sulfate-polyacrylamide gel electrophoresisSDS-PAGETerminal deoxynucleotidyl transferase-mediated dUTP nick end labelingTUNELDimethylsulfoxideDulbecco's modified Eagle's mediaSODfetal bovine serumSuperoxide dismutaseextracellular signal regulated kinasePhosphate-buffered salinePARP inhibitorCatalasemitogen-activated protein kinasesReactive oxygen species
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Authors
Eun-Seok Park, Jun Chul Kang, Do-Hyun Kang, Yong Chang Jang, Kyu Yang Yi, Hun-Jong Chung, Jong Seok Park, Bokyung Kim, Zhong-Ping Feng, Hwa-Sup Shin,