Levo-tetrahydropalmatine Attenuates Neuron Apoptosis Induced by Cerebral Ischemia –Reperfusion Injury: Involvement of c-Abl Activation

AbstractIschemic stroke is one of the most dangerous acute diseases which causes death or deformity. Apoptosis has been shown to play an important role in the development and pathogenesis of cerebral ischemia –reperfusion injury (I/R injury), but the related mechanism is unclear. Levo-tetrahydropalmatine (l-THP), a bioactive ingredient extracted from the Chinese herbCorydalis, can penetrate the blood –brain barrier and exert various pharmacological effects on neural tissues. The present study examined the neuroprotective effect ofl-THP on neuronal apoptosis induced by cerebral I/R injury. Results showed that pretreatment withl-THP (12.5, 25, and 50  mg/kg) improved neurological outcomes and reduced infarct volume and cerebral edema in comparison with the brains of the middle cerebral artery occlusion (MCAO) group. These findings provided evidence for the neuroprotective effects ofl-THP against cerebral I/R injury. Furthermore, administration ofl-THP enhanced the expression of Bcl-2 and attenuated the content of Bax, cleaved caspase-3, and PARP.l-THP could improve the reduction of NeuN-positive cells induced by I/R injury. These results suggested thatl-THP could inhibit neuroapoptosis in cerebral ischemic rats. c-Abl was discovered as the critical protein responsible for neurocyte apoptosis; however, few data have been published on the relation between ischemic stroke and the expression of c-Abl. We found that both c-Abl expression and neuronal apoptosis were significantl...
Source: Journal of Molecular Neuroscience - Category: Neuroscience Source Type: research