【摘 要】
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The present study sought to investigate mechanisms by which p53 induction contributes to excitotoxic neuronal injury.Rats were intrastriatally administered
【机 构】
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Department of Pharmacology and Laboratory of Aging and Nervous Diseases(SZS0703), Soochow University
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The present study sought to investigate mechanisms by which p53 induction contributes to excitotoxic neuronal injury.Rats were intrastriatally administered the N-methyl-d-aspartate (NMDA) receptor agonist quinolinic acid (QA),the changes in the expression of p53 and its target genes involved in apoptosis and autophagy,including p53-upregulated modulator of apoptosis (PUMA),Bax,Bcl-2,damage-regulated autophagy modulator (DRAM) and other autophagic proteins including microtubule-associated protein 1 light chain 3 (LC3) and beclin 1 were assessed.The contribution of p53-mediated autophagy activation to apoptotic death of striatal neurons was assessed with co-administration of the nuclear factor-kappaB (NF-κB) inhibitor SNS0,the p53 inhibitor Pifithrin-alpha (PFT-α) or the autophagy inhibitor 3-methyladenine (3-MA).
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