Neuroprotective action of dextromethorphan in rat photochemically-induced focal cerebral ischemia
Abstract
AIM: To study the effects of dextromethorphan (Dex) on photochemically-induced focal cerebral ischemia in rats.
METHODS: Anesthetized rats undergone 10-min light irradiation on exposed skull after rose bengal injection were pretreated with saline and Dex at 3 doses (12.5, 25, and 50 mg.kg-1, i.p., 15 min before ischemia). The alteration of volume of lesioned cortical region, regional cerebral blood flow (CBF), bcl-2 and bax expression at penumbra area were studied.
RESULTS: Dex dose-dependently decreased the infarcted volume (17%, 26%, and 50% reduction, respectively). Pretreatment with Dex at a dose of 50 mg.kg-1 improved the postischemic hypoperfusion compared with the control at 20 and 30 min after lesion (both 31% increase), and also upregulated the expression of anti-apoptosis gene bcl-2.
CONCLUSION: Dex protects against ischemic neuronal damage in this model and its effects on CBF and bcl-2 expression may contribute to its neuroprotective action.
Keywords:
METHODS: Anesthetized rats undergone 10-min light irradiation on exposed skull after rose bengal injection were pretreated with saline and Dex at 3 doses (12.5, 25, and 50 mg.kg-1, i.p., 15 min before ischemia). The alteration of volume of lesioned cortical region, regional cerebral blood flow (CBF), bcl-2 and bax expression at penumbra area were studied.
RESULTS: Dex dose-dependently decreased the infarcted volume (17%, 26%, and 50% reduction, respectively). Pretreatment with Dex at a dose of 50 mg.kg-1 improved the postischemic hypoperfusion compared with the control at 20 and 30 min after lesion (both 31% increase), and also upregulated the expression of anti-apoptosis gene bcl-2.
CONCLUSION: Dex protects against ischemic neuronal damage in this model and its effects on CBF and bcl-2 expression may contribute to its neuroprotective action.