Effect of P-hydroxycinnamic acid in mice model of cerebral ischemia-reperfusion injury

Multiple pathomechanisms of cerebral ischemia reperfusion (I/R) injuries can be ameliorated by certain high-potential pharmaceutical substances. In the present study, we investigated the acute effect of p-hydroxycinnamic (pHCA) acid against cerebral I/R injury in mice. Thirty male ICR mice were divi...

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Bibliographic Details
Main Authors: Romgase Sakamula, Chanikarn Sakdapitak, Wachiryah Thong-asa
Format: Article
Language:English
Published: Penerbit Universiti Kebangsaan Malaysia 2019
Online Access:http://journalarticle.ukm.my/14401/
http://journalarticle.ukm.my/14401/
http://journalarticle.ukm.my/14401/1/18%20Romgase%20Sakamula.pdf
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Summary:Multiple pathomechanisms of cerebral ischemia reperfusion (I/R) injuries can be ameliorated by certain high-potential pharmaceutical substances. In the present study, we investigated the acute effect of p-hydroxycinnamic (pHCA) acid against cerebral I/R injury in mice. Thirty male ICR mice were divided into Sham, Control-I/R, and pHCA-I/R groups. The pHCA 100 mg/kg and the vehicle were given 30 min before I/R induction. Thirty-minute bilateral common carotid artery occlusion followed by 45-min reperfusion was performed on the Control-I/R and pHCA-I/R groups. Brains were collected for biochemical analysis, infarction and histological study of the cerebral cortex and corpus callosum (CC). The results showed that I/R induction significantly induced biochemical changes (p<0.05) along with the increase of brain infarction (p<0.05), percentage of degeneration in cerebral cortex (p<0.05) and decrease of CC white matter density (p<0.05). Pretreatment with pHCA significantly reduced MDA (p<0.05), brain infarction (p<0.05), cerebral cortex neuronal degeneration (p<0.05) and prevented the reduction of white matter density in the CC (p<0.05). The present study concluded that pretreatment with pHCA helps prevent cerebral I/R injury by amelioration of lipid peroxidation, white matter damage and neuronal degeneration.