Thioperamide treats neonatal hypoxic-ischemic encephalopathy by postsynaptic H1 receptors*

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Abstract

Research Highlights

(1) The mechanism underlying the ability of thioperamide, a selective histamine H3 receptor gonist, to improve neonatal hypoxic-ischemic encephalopathy was investigated to determine if this compound could be a novel therapy for this condition.

Research Highlights

(2) A combined application of thioperamide with H1 and H2 receptor antagonists showed that the action of increased brain histamine was mediated through postsynaptic H1 receptors.

Thioperamide, a selective histamine H3 receptor antagonist, can increase histamine content in the brain, improve brain edema, and exert a neuroprotective effect. This study aimed to examine the mechanism of action of thioperamide during brain edema in a rat model of neonatal hypoxic-ischemic encephalopathy. Our results showed that thioperamide significantly decreased brain water content and malondialdehyde levels, while significantly increased histamine levels and superoxide dismutase activity in the hippocampus. This evidence demonstrates that thioperamide could prevent oxidative damage and attenuate brain edema following neonatal hypoxic-ischemic encephalolopathy. We further observed that changes in the above indexes occurred after combined treatment of thioperamide with the H1 receptor antagonist, pyrilamine, and the H2 receptor antagonist, tidine. Experimental findings indicated that pyrilamine reversed the effects of thioperamide; however, cimetidine had no significant influence on the effects of thioperamide. Our present findings suggest that thioperamide can increase brain histamine content and attenuate brain edema and oxidative damage by acting in combination with postsynaptic H1 receptors in a rat model of neonatal ic-ischemic encephalopathy.

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