Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5846935 | Toxicology and Applied Pharmacology | 2011 | 11 Pages |
Abstract
âºPQQ attenuated glutamate-induced cell apoptosis of cultured hippocampal neurons. âºPQQ inhibited glutamate-induced Ca2+ influx and caspase-3 activity. âºPQQ reduced glutamate-induced increase in ROS production. âºPQQ affected phosphorylation of Akt and JNK signalings after glutamate injury. âºPI3K/Akt was required for neuroprotection of PQQ by modulating Bcl-2/Bax ratio.
Keywords
CREBNMDATFAMAMPAN-methyl-d-aspartic acidDTNBPQQNRFERKWST-8MDAPyrroloquinoline quinineJnk5,5′-Dithio-bis (2-nitrobenzoic acid)terminal deoxynucleotidyl transferase biotin-dUTP nick end labelingCCK-8PI3Knuclear respiratory factorsAKT signalingc-Jun N-terminal protein kinaseMAPKROSTUNELApoptosisSODSuperoxide dismutasecell counting kit-8mitochondrial transcription factor Aphosphatidylinositol-3-kinasemalondialdehydeHippocampal neuronsNitric oxidecAMP response element binding proteinmitogen activated protein kinasePropidium iodidePyrroloquinoline quinoneKainiteextracellular signal-regulated kinasesglutamateReactive oxygen species
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Authors
Qi Zhang, Mi Shen, Mei Ding, Dingding Shen, Fei Ding,