Effect of beraprost sodium (BPS) on the postischemic neuropathological changes and stroke index after left carotid artery occlusion in gerbils

Ueno, Shinji; Miyauchi, Yasushi; Matsuda, Susumu; Endoh, Takashi

doi:10.1007/bf02815407

Cited by 2 publications

(1 citation statement)

References 19 publications

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“…Beraprost is the first PGI2 analogue available as an oral formulation to protect against pulmonary arterial hypertension in humans [ 10 ]. Beraprost has been reported to protect against left carotid artery occlusion induced hippocampal CA1 brain injury in gerbils [ 11 ] and to prevent nephropathy via phosphorylation of cyclic AMP response element binding (CREB) protein [ 12 ], which is also involved in learning and memory and ischemic tolerance [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice

Shakil

Saleem

2015

J Neurol Disord

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Beraprost sodium is a new stable, orally active Prostaglandin I2 analogue. The aim of this study was to determine the effect of beraprost on cognitive dysfunction and locomotor impairment induced by bilateral common carotid artery occlusion in mice. We investigated the ameliorating effect of beraprost through PGI2 IP receptor by studying neurologic deficit assessment and T-maze testing in young and old male C57Bl/6 wild-type (WT) and IP receptor knockout (IP KO) mice following a 12 min bilateral common carotid artery occlusion (BCCAo) and 7 days of reperfusion. Beraprost reversed BCCAo induced cognitive impairment and neurological deficit in a dose dependent manner. Immunohistochemical studies showed attenuation of neuronal cell death, astrogliosis, microglial invasion, and myeloperoxidase (MPO) activity in both young and old WT mice after post treatment with beraprost. Moreover, after BCCAo, phosphorylated cAMP response element binding protein positive cell numbers were increased with beraprost treatment over vehicle treated controls. These results show that beraprost treatment attenuated cognitive dysfunction and neurological deficits induced by BCCAo, and suggest that this effect may be mediated by the neuroprotective effects of treatment.

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Section: Introductionmentioning

confidence: 99%

Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice

Shakil

Saleem

2015

J Neurol Disord

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Effect of beraprost sodium (BPS), a prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced chronic cortical atrophy in gerbils

Ueno

Miyauchi

Izumimoto

et al. 1994

Molecular and Chemical Neuropathology

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We investigated the effect of beraprost sodium (BPS), a new prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced cerebral atrophy and chronic cortical neuronal loss in gerbils. The left common carotid artery of gerbils was repeatedly occluded (for 10, 7, 7, and 7 min) at intervals of 24 h. The thickness of the cerebral cortex of the ischemic hemisphere diminished with increasing time of reperfusion after an ischemic insult. The animals were given BPS (1-100 micrograms/kg, po) or MK-801 (3-300 micrograms/kg, sc) after the first ischemic insult, and then twice daily for 4 wk. Increases in the amount of neuronal loss and acidophilic neurons, and progressive atrophy were observed with increasing time of reperfusion in the cerebral cortex of the ischemic hemisphere. Cortical sections revealed no astrocytes positive for glial fibrillary acidic protein (GFAP), whereas the hippocampal CA1 area showed neuronal loss accompanied by GFAP-positive astrocytes. In control animals at 4 wk survival, the area ratio (area of ischemic cortex/area of opposite cortex) and the cortical neurons ratio (number of neurons in ischemic cortex/number of neurons in opposite cortex) were 89.8 +/- 3.0% and 74.6 +/- 3.4%, respectively. BPS was found to inhibit atrophy and chronic cortical neuronal loss in the ischemic hemisphere in a dose-dependent manner, whereas MK-801 showed no inhibitory effects at any dose tested. These results may suggest that the nature of neuronal degeneration differs between the cortical and hippocampal areas, that cortical neuronal degeneration might not involve glutamate pathways with NMDA receptors in this model, and that prostacyclin could play an essential role in prevention of ischemia-induced progressive neuronal loss.

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Effect of beraprost sodium (BPS) on the postischemic neuropathological changes and stroke index after left carotid artery occlusion in gerbils

Cited by 2 publications

References 19 publications

Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice

Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice

Effect of beraprost sodium (BPS), a prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced chronic cortical atrophy in gerbils

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