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Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation
Author(s) -
Shen Yao,
Zhang Shihong,
Fu Lin,
Hu Weiwei,
Chen Zhong
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1447
Subject(s) - degranulation , carnosine , histamine , mast cell , chemistry , compound 48/80 , liberation , histamine n methyltransferase , endogeny , pharmacology , biochemistry , biology , immunology , histamine h2 receptor , in vitro , receptor , antagonist
Abstract Carnosine ( β ‐alanyl‐histidine) is a naturally occurring dipeptide that has been characterized as a putative hydrophilic antioxidant. The protective function of carnosine has been demonstrated in neuronal cells under ischemic injury. The purpose of this study was to investigate the effects of carnosine on oxygen–glucose deprivation (OGD)‐induced degranulation and histamine release from mast cells. Cultured mast cells were exposed to OGD for 4 h, and then the degranulation was observed immediately by microscopy. Histamine release was analyzed by high‐performance liquid chromatography (HPLC). OGD caused degranulation of mast cells, and increased histamine and lactate dehydrogenase (LDH) release. Carnosine (at a concentration of 5 mM) alone did not produce any appreciable effect on degranulation, histamine, and LDH release from mast cells under normal condition, but significantly inhibited the degranulation, histamine, and LDH release of mast cells induced by OGD. These results indicate that carnosine can protect mast cells from degranulation and histamine release and it may be an endogenous mast cell stabilizer in the pathological processes induced by ischemia. Copyright © 2007 John Wiley & Sons, Ltd.