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Exacerbated brain damage, edema and inflammation in type‐2 diabetic mice subjected to focal ischemia
Author(s) -
Tureyen Kudret,
Bowen Kellie,
Liang Jin,
Dempsey Robert J.,
Vemuganti Raghu
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.07127.x
Subject(s) - medicine , proinflammatory cytokine , ischemia , neuroprotection , inflammation , stroke (engine) , middle cerebral artery , diabetes mellitus , edema , occlusion , brain damage , type 2 diabetes , endocrinology , anesthesia , mechanical engineering , engineering
J. Neurochem. (2011) 116 , 499–507. Abstract One of the limiting factors in stroke therapeutic development is the use of animal models that do not well represent the underlying medical conditions of patients. In humans, diabetes increases the risk of stroke incidence as well as post‐stroke mortality. To understand the mechanisms that render diabetics to increased brain damage, we evaluated the effect of transient middle cerebral artery occlusion in adult db/db mice. The db/db mouse is a model of type‐2 diabetes with four times higher blood sugar than its normoglycemic genetic control( db/+ mouse). Following transient middle cerebral artery occlusion, the db/db mice showed significantly higher mortality, bigger infarcts, increased cerebral edema, worsened neurological status compared to db/+ mice. The db/db mice also showed significantly higher post‐ischemic inflammatory markers (ICAM1 + capillaries, extravasated macrophages/neutrophils and exacerbated proinflammatory gene expression) compared to db/+ mice. In addition, the post‐ischemic neuroprotective heat‐shock chaperone gene expression was curtailed in the db/db compared to db/+ mice.