摘要
Background The underlying mechanism of early neurobiological impairment after subarachnoid hemorrhage （SAH） is not well understood, but the system of reactive oxygen superoxide （ROS） might be involved. Edaravone （MCI-186）, a potent free radical scavenger that prevents apoptosis of neurons, was thus used in this study to see its possible therapeutic effect in early brain injury due to SAH in a rat model. Methods One hundred and twenty male Sprague-Dawley rats were randomly assigned to four groups： group 1, control rats receiving sham operation only; group 2, rats with SAH treated by saline; group 3, rats with SAH treated with 1 mg/kg MCI-186 injected intraperitoneally; and group 4, rats with SAH treated with 3 mg/kg MCI-186. Treated with either saline or MCI-186 twice daily for two consecutive days after SAH, the rats were sacrificed for measurements of malondialdehyde （MDA） and activity of superoxide dismutase （SOD） and histological analysis of caspase-3 protein by Western blotting and immunohistochemical staining. In addition, mortality and neurological scores were statistically analyzed by the chi-square test and Dunn＇s procedure respectively for each group. One-way analysis of variance followed by the Tukey＇s procedure was also used in data analysis. Results The rats in group 2 that received saline only showed neurological impairment as well as elevated mortality, and were found to have significantly increased levels of MDA and caspase-3, but reduced SOD activities in brain tissues （P 〈0.05）. When treated with MCI-186 at two different dosages, the rats in groups 3 and 4 had markedly decreased levels of MDA and caspase-3 but increased SOD activities in the brain tissue （P 〈0.05）, along with improved scores of neurological evaluation （P 〈0.05）. Conclusions This study sheds some lights on the therapy of SAH-induced early brain injury by providing the promising data indicating that MCI-186, a radical scavenger, can efficiently diminish apoptosis of neurons and thus preve
Background The underlying mechanism of early neurobiological impairment after subarachnoid hemorrhage （SAH） is not well understood, but the system of reactive oxygen superoxide （ROS） might be involved. Edaravone （MCI-186）, a potent free radical scavenger that prevents apoptosis of neurons, was thus used in this study to see its possible therapeutic effect in early brain injury due to SAH in a rat model. Methods One hundred and twenty male Sprague-Dawley rats were randomly assigned to four groups： group 1, control rats receiving sham operation only; group 2, rats with SAH treated by saline; group 3, rats with SAH treated with 1 mg/kg MCI-186 injected intraperitoneally; and group 4, rats with SAH treated with 3 mg/kg MCI-186. Treated with either saline or MCI-186 twice daily for two consecutive days after SAH, the rats were sacrificed for measurements of malondialdehyde （MDA） and activity of superoxide dismutase （SOD） and histological analysis of caspase-3 protein by Western blotting and immunohistochemical staining. In addition, mortality and neurological scores were statistically analyzed by the chi-square test and Dunn＇s procedure respectively for each group. One-way analysis of variance followed by the Tukey＇s procedure was also used in data analysis. Results The rats in group 2 that received saline only showed neurological impairment as well as elevated mortality, and were found to have significantly increased levels of MDA and caspase-3, but reduced SOD activities in brain tissues （P 〈0.05）. When treated with MCI-186 at two different dosages, the rats in groups 3 and 4 had markedly decreased levels of MDA and caspase-3 but increased SOD activities in the brain tissue （P 〈0.05）, along with improved scores of neurological evaluation （P 〈0.05）. Conclusions This study sheds some lights on the therapy of SAH-induced early brain injury by providing the promising data indicating that MCI-186, a radical scavenger, can efficiently diminish apoptosis of neurons and thus preve
