Tert-butylhydroquinone alleviates early brain injury and cognitive dysfunction after experimental subarachnoid hemorrhage: Role of Keap1/Nrf2/ARE pathway

PLoS ONE

Volumn 9, Issue 5, 2014, Pages

  Wang, Zhong ^a   Ji, Chengyuan ^a   Wu, Lingyun ^a   Qiu, Jiaoxue ^a   Li, Qi ^a   Shao, Zhong ^a   Chen, Gang ^a  

^a SOOCHOW UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

GLUTATHIONE TRANSFERASE ALPHA; GLUTATHIONE TRANSFERASE ALPHA1; HEME OXYGENASE 1; KELCH LIKE ECH ASSOCIATED PROTEIN 1; MESSENGER RNA; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE (PHOSPHATE) DEHYDROGENASE (QUINONE); REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE (PHOSPHATE) DEHYDROGENASE (QUINONE) 1; TERT BUTYLHYDROQUINONE; TRANSCRIPTION FACTOR NRF2; UNCLASSIFIED DRUG; 2-TERT-BUTYLHYDROQUINONE; DNA; GLUTATHIONE S-TRANSFERASE ALPHA; GLUTATHIONE TRANSFERASE; HYDROQUINONE DERIVATIVE; ISOENZYME; KEAP1 PROTEIN, RAT; NEUROPROTECTIVE AGENT; NQO1 PROTEIN, RAT; SIGNAL PEPTIDE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT RESPONSIVE ELEMENT; APOPTOSIS; ARTICLE; BRAIN CORTEX; BRAIN DEGENERATION; BRAIN EDEMA; BRAIN INJURY; COGNITIVE DEFECT; CONTROLLED STUDY; DRUG MECHANISM; GENE EXPRESSION; HISTOPATHOLOGY; LEARNING DISORDER; MEMORY DISORDER; MORRIS WATER MAZE TEST; NEUROPROTECTION; NONHUMAN; OXIDATIVE STRESS; PROTEIN DNA BINDING; PROTEIN EXPRESSION; RAT; SIGNAL TRANSDUCTION; SUBARACHNOID HEMORRHAGE; ANIMAL; ANIMAL BEHAVIOR; BRAIN; BRAIN INJURIES; COGNITION; COMPLICATION; DRUG EFFECTS; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; SPRAGUE DAWLEY RAT;

ANIMALS; ANTIOXIDANT RESPONSE ELEMENTS; APOPTOSIS; BEHAVIOR, ANIMAL; BRAIN; BRAIN INJURIES; COGNITION; DNA; GENE EXPRESSION REGULATION; GLUTATHIONE TRANSFERASE; HEME OXYGENASE-1; HYDROQUINONES; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; ISOENZYMES; NAD(P)H DEHYDROGENASE (QUINONE); NEUROPROTECTIVE AGENTS; NF-E2-RELATED FACTOR 2; OXIDATIVE STRESS; RATS; RATS, SPRAGUE-DAWLEY; RNA, MESSENGER; SIGNAL TRANSDUCTION; SUBARACHNOID HEMORRHAGE;

EID: 84901366903     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0097685     Document Type: Article

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