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The alpha1 adrenoreceptor antagonist tamsulosin is primarily used to treat benign prostatic hypertrophy. In this study, we intragastrically administered rats with 0.01, 0.1 and 1 mg/kg tamsulosin to investigate the effects of tamsulosin on memory function, and hippocampal cell apoptosis and proliferation following intracerebral hemorrhage. Step-down avoidance task re-sults showed that tamsulosin treatment markedly alleviated intracerebral hemorrhage- induced short-term memory impairment. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling results showed that tamsulosin treatment markedly suppressed intracerebral hemorrhage-induced caspase-3 expression in the hippocampal CA1 region and cell prolifera-tion in the hippocampal dentate gyrus. Tamsulosin treatment at a dose of 0.01 mg/kg exhibited the most potent inhibitory effects on cell apoptosis and proliferation. These findings suggest that tamsulosin treatment facilitates the recovery of rat memory function by inhibiting hippo-campal cell apoptosis and proliferation following intracerebral hemorrhage.
The alpha1 adrenoreceptor antagonist tamsulosin is primarily used to treat benign prostatic hypertrophy. In this study, we intragastrically administered rats with 0.01, 0.1 and 1 mg / kg tamsulosin to investigate the effects of tamsulosin on memory function, and hippocampal cell apoptosis and proliferation following intracerebral hemorrhage. Step-down avoidance task re-sults showed that tamsulosin treatment markedly alleviated intracerebral hemorrhage- induced short-term memory impairment. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling results showed that tamsulosin treatment markedly suppressed intracerebral hemorrhage-induced caspase- 3 expression in the hippocampal CA1 region and cell prolifera tion in the hippocampal dentate gyrus. Tamsulosin treatment at a dose of 0.01 mg / kg exhibited the most potent inhibitory effects on cell apoptosis and proliferation. These findings suggest that tamsulosin treatment facilitates the recovery of rat memory function by inhibit ing hippo-campal cell apoptosis and proliferation following intracerebral hemorrhage.