【摘要】 目的　探讨二氢石蒜碱 (DL)对大鼠海马脑片缺糖缺氧损伤的影响。方法　在大鼠离体海马脑片上 ,应用细胞外记录技术 ,记录CAl1区群峰电位 ,以群峰电位 (PS)持续时间以及恢复程度作为判断药效标准。结果　对照组及二氢石蒜碱组PS持续时间分别为 335 .13± 74.73s和 76 1.5 0± 2 6 8.30s,显示DL组缺糖缺氧后PS持续时间明显延长 (与对照组比较P <0 .0 5 ) ,而哌唑嗪在 1× 10 -6mol·L-1时无影响 ,持续缺糖缺氧 7min30s后 ,对照组PS幅度为 4.93%± 7.78% ,而DL(1× 10 -6mol·L-1)组仍保持 48.2 2 %±2 7.0 8% ;复糖复氧 10minDL(1× 10 -6mol·L-1及 1× 10 -5mol·L-1)组PS恢复较对照组好 (P <0 .0 5 ) ,对照组、DL(1× 10 -6mol·L-1)组、DL(1× 10 -5mol·L-1)组及酚妥拉明 (5× 10 -5mol·L-1)组PS分别恢复到缺糖缺氧前 14.17%± 34 .70 %、94.30 %± 49.10 %、71.0 0 %± 41.40 %、71.40 %± 46 .0 2 %。结论　DL对海马脑片缺糖缺氧损伤有明显的保护作用。其机理可能是为DL阻滞肾上腺素能受体及改善能量代谢 ,从而提高了海马脑片抗缺氧缺糖损伤的能力。更多还原

【Abstract】 Objective To investigate the effect of dihydrolycorine on hippocampal slices injury induced hypoglycemia and anoxia. Methods The microelectrode recording technology was used to record the stimulus evoked population spikes in CAl 1 region of rat hippocampal slices, the effect was determined by the change and the sustained time of population spikes during hypoglycemia and anoxia or recovery percentage of population spikes after reperfusion. Results The sustained time(sec) of control and DL groups were 335.13 ± 74.13 s、 761.50 ± 268.30 s respectively, which showed that DL had longer sustained time of population spikes than the control, but prazosin(1×10 -6 mol·L -1 ) had no effect. The amplitude of population spike of controls decreased to 4.39 %± 7.78 %, while the DL(1×10 -6 mol·L -1 ) group kept up to 48.22 %± 27.08 % after anoxia and hypoglycemia for 7 minutes 30 seconds. After reperfusion with ACSF(the component is same as that of prehypoglycemia and anoxia)for 10 minutes the recovery percentage of the DL(1×10 -6 mol·L -1 、 1×10 -5 mol·L -1 )and phentolamine(5×10 -5 mol·L -1 )groups 94.30 %± 49.10 %、 71.00 %± 41.40 %、 71.40 %± 46.02 % respectively)was higher than the controls( 14.17 %± 34.70 %). Conclusion The present data demonstrated that dihydrolycorine effectively prevent from the irreversible injury of neurons during anoxia and hypoglycemia which suggested that the DL should provide significantly protection against anoxic and hypoglycemia injury for hippocampal slices. The mechanism may be DL block of α and β receptor and improve of the energy metabolism.更多还原