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Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

机译:神经甾体调节对小鼠全脑缺血再灌注致脑损伤的影响

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摘要

The present study was designed to investigate the putative effect of neurosteroid modulation on global ischaemia-reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion followed by reperfusion, produced a significant rise in cerebral infarct size along with impairment of grip strength and motor coordination in Swiss albino mice. Administration of carbamazepine (16 mg/kg, i.p.) before global cerebral ischaemia significantly attenuated cerebral infarct size and improved the motor performance. However, administration of indomethacin (100 mg/kg, i.p.) attenuated the neuroprotective effect of carbamazepine. Mexiletine (50 mg/kg, i.p.) did not produce significant neuroprotective effect. It may be concluded that the neuroprotective effect of carbamazepine may be due to increase in synthesis of neurosteroids perhaps by activating enzyme (3α HSD) as indomethacin attenuated the neuroprotective effect of carbamazepine. The sodium channel blocking effect of carbamazepine may not be involved in neuroprotection as mexiletine, a sodium channel blocker, did not produce significant neuroprotective effect.
机译:本研究旨在研究神经甾体调节对小鼠全脑缺血再灌注所致脑损伤的假定作用。在瑞士的白化病小鼠中,双侧颈动脉闭塞后再灌注,导致脑梗死面积明显增加,以及握力和运动协调能力受损。在全局性脑缺血之前给予卡马西平(16 mg / kg,腹腔注射)可显着减轻脑梗死面积并改善运动表现。然而,消炎痛的给药(100 mg / kg,腹腔注射)减弱了卡马西平的神经保护作用。美西律(50 mg / kg,i.p.)没有产生明显的神经保护作用。可以得出结论,卡马西平的神经保护作用可能是由于神经甾类化合物的合成增加,可能是由于吲哚美辛减弱了卡马西平的神经保护作用而激活了酶(3αHSD)。卡马西平的钠通道阻滞作用可能不参与神经保护作用,因为美西律汀(一种钠通道阻滞剂)未产生明显的神经保护作用。

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