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l histidine/infarci
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Reduction of the infarct size by simultaneous administration of L-histidine and diphenhydramine in ischaemic rat brains.
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OBJECTIVE
While diphenhydramine is a histamine H(1) receptor antagonist, the agent has been shown to inhibit histamine-N-methyltransferase, a histamine inactivating enzyme in the brain. Since an increase in the brain concentration of histamine ameliorates reperfusion injury after cerebral ischaemia,
Reduction in brain infarction by augmentation of central histaminergic activity in rats.
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Inflammation is a factor in the aggravation of reperfusion injury after cerebral ischemia. Since histamine H(2) receptor stimulation suppresses inflammatory reactions, effects of the central histaminergic activation on brain infarction were examined in rats. Focal cerebral ischemia for 2 h was
β-alanine and L-histidine supplementation associated with combined training increased functional capacity and maximum strength in heart failure rats.
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Combined training (CT) has been associated with positive responses in the clinical status of patients with chronic heart failure (CHF). Other non-pharmacological tools, such as amino acid supplementation, may further enhance its adaptation. However, the effects of β-alanine and L-histidine
Differential neuroprotective effects of carnosine, anserine, and N-acetyl carnosine against permanent focal ischemia.
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Carnosine (beta-alanyl-L-histidine) has been shown to exhibit neuroprotection in rodent models of cerebral ischemia. In the present study, we further characterized the effects of carnosine treatment in a mouse model of permanent focal cerebral ischemia and compared them with its related peptides
Targeted disruption of organic cation transporter 3 (Oct3) ameliorates ischemic brain damage through modulating histamine and regulatory T cells.
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The organic cation transporters OCT1, 2, and 3 (SLC22A1-3) have been implicated in the elimination of biogenic amines such as histamine. Among them, OCT3 was identified as an uptake-2 transporter, responsible for clearance of histamine. Because increasing evidence suggests the involvement of
Alleviation of ischemia-induced brain edema by activation of the central histaminergic system in rats.
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We have reported that facilitation of central histaminergic activity prevents the development of ischemia-induced brain injury. Since cerebral edema is a major cause of brain damage, we studied effects on brain edema of postischemic administration of L-histidine, a precursor of histamine, and
Exploring the effects of Gastrodia elata Blume on the treatment of cerebral ischemia-reperfusion injury using UPLC-Q/TOF-MS-based plasma metabolomics.
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Gastrodia elata Blume (Orchidaceae, GEB) is a medicinal plant that has been widely used in the treatment of cerebrovascular disease. This study explored the protective effects of GEB against cerebral ischemia-reperfusion using Information-Dependent Acquisition (IDA)-mediated UPLC-Q/TOF-MS-based
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