Suppression of inflammatory cell recruitment by histamine receptor stimulation in ischemic rat brains

Hiraga, Norihito; Adachi, Naoto; Liu, Keyue; Nagaro, Takumi; Arai, T.

doi:10.1016/j.ejphar.2006.11.020

Cited by 44 publications

(28 citation statements)

References 46 publications

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“…28 An early increase in endogenous histamine, which is produced by histamine release from mast cells and basophils in allergic inflammation, is related to allergic reactions by enhancing vascular permeability and edema formation through histamine H 1 receptors. 29 Since carnosine can inhibit mast cell degranulation and histamine release induced by OGD, it is reasonable to propose that carnosine, through inhibiting histamine release from mast cells to attenuate allergic inflammation, subsequently exerts its protection against ischemic injury.…”

Section: Resultsmentioning

confidence: 99%

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Shen

Zhang

et al. 2007

Cell Biochemistry & Function

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Carnosine (beta-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.

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Section: Resultsmentioning

confidence: 99%

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Shen

Zhang

et al. 2007

Cell Biochemistry & Function

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“…Histamine H 2 action reduced inflammatory cell recruitment during reperfusion phase and ameliorated brain damage caused by transient ischemia [14,15]. In the liver, histamine H 4 action reduced production of proinflammatory cytokines and suppressed ischemia-induced liver damage [16][17][18].…”

Section: Discussionmentioning

confidence: 98%

Suppression of peritoneal thickening by histamine in a mouse model of peritoneal scraping

Liu

Yorozuya

Adachi³

et al. 2014

Clin Exp Nephrol

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“…Simultaneous administration of thioperamide further decreases this number to 32%. 68 Likewise, the ischemia-induced increase in the number of CD68-positive cells (including polymorphonuclear leukocytes and macrophages/microglia) after 24 h is suppressed by L-histidine injection. The L-histidine administration decreases the number of CD4 + T lymphocytes on both the ischemic and contralateral sides after 12 h, and concurrent administration of thioperamide prolongs the effect.…”

Section: ■ Possible Mechanisms By Which Histaminementioning

confidence: 96%

Role of Histamine and Its Receptors in Cerebral Ischemia

Chen

2012

ACS Chem. Neurosci.

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Histamine is recognized as a neurotransmitter or neuromodulator in the brain, and it plays a major role in the pathogenic progression after cerebral ischemia. Extracellular histamine increases gradually after ischemia, and this may come from histaminergic neurons or mast cells. Histamine alleviates neuronal damage and infarct volume, and it promotes recovery of neurological function after ischemia; the H1, H2, and H3 receptors are all involved. Further studies suggest that histamine alleviates excitotoxicity, suppresses the release of glutamate and dopamine, and inhibits inflammation and glial scar formation. Histamine may also affect cerebral blood flow by targeting to vascular smooth muscle cells, and promote neurogenesis. Moreover, endogenous histamine is an essential mediator in the cerebral ischemic tolerance. Due to its multiple actions, affecting neurons, glia, vascular cells, and inflammatory cells, histamine is likely to be an important target in cerebral ischemia. But due to its low penetration of the blood-brain barrier and its wide actions in the periphery, histamine-related agents, like H3 antagonists and carnosine, show potential for cerebral ischemia therapy. However, important questions about the molecular aspects and pathophysiology of histamine and related agents in cerebral ischemia remain to be answered to form a solid scientific basis for therapeutic application.

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Suppression of inflammatory cell recruitment by histamine receptor stimulation in ischemic rat brains

Cited by 44 publications

References 46 publications

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Suppression of peritoneal thickening by histamine in a mouse model of peritoneal scraping

Role of Histamine and Its Receptors in Cerebral Ischemia

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