Overproduction of nitric oxide intensifies brain infarction and cerebrovascular damage through reduction of claudin-5 and ZO-1 expression in striatum of ischemic brain

Pathology Research and Practice

Volumn 212, Issue 11, 2016, Pages 959-964

  Mohammadi, Mohammad Taghi ^a  

^a BAQIYATALLAH UNIVERSITY OF MEDICAL SCIENCES   (Iran)

Author keywords

Brain ischemia; Claudin 5; L NAME; Nitric oxide; Zonula occludens 1

Indexed keywords

CLAUDIN 5; MESSENGER RNA; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; PROTEIN ZO1; CLDN5 PROTEIN, RAT; TJP1 PROTEIN, RAT;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN INFARCTION; BRAIN INFARCTION SIZE; BRAIN ISCHEMIA; BRAIN NERVE CELL; CEREBROVASCULAR DISEASE; CLAUDIN 5 GENE; CONTROLLED STUDY; CORPUS STRIATUM; HISTOPATHOLOGY; MALE; MIDDLE CEREBRAL ARTERY OCCLUSION; NONHUMAN; PROTEIN EXPRESSION; RAT; REPERFUSION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; ZO 1 GENE; ANIMAL; BIOSYNTHESIS; CAPILLARY PERMEABILITY; DISEASE MODEL; METABOLISM; PATHOLOGY; PHYSIOLOGY; SPRAGUE DAWLEY RAT;

ANIMALS; BRAIN INFARCTION; CAPILLARY PERMEABILITY; CLAUDIN-5; CORPUS STRIATUM; DISEASE MODELS, ANIMAL; MALE; NITRIC OXIDE; RATS; RATS, SPRAGUE-DAWLEY; ZONULA OCCLUDENS-1 PROTEIN;

EID: 84994493964     PISSN: 03440338     EISSN: 16180631     Source Type: Journal    
DOI: 10.1016/j.prp.2015.12.009     Document Type: Article

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