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Neuroprotection with a calpain inhibitor in a model of focal cerebral ischemia.
Author(s) -
SeungChyul Hong,
Yasunobu Goto,
Giuseppe Lanzino,
Scott W. Soleau,
Neal F. Kassell,
Kevin S. Lee
Publication year - 1994
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.25.3.663
Subject(s) - calpain , medicine , ischemia , neuroprotection , saline , infarction , proteolysis , calcium , brain ischemia , anesthesia , middle cerebral artery , endocrinology , pathology , pharmacology , biochemistry , myocardial infarction , biology , enzyme
Excessive elevation of intracellular calcium and uncontrolled activation of calcium-sensitive events are believed to play a central role in ischemic neuronal damage. Calcium-activated proteolysis by calpain is a candidate to participate in this form of pathology because it is activated under ischemic conditions and its activation results in the degradation of crucial cytoskeletal and regulatory proteins. The present studies examined the effects of a cell-penetrating inhibitor of calpain on the pathological outcome after transient focal ischemia in the brain.

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