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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。
Objective To investigate the effects of dihydropalcinate (DL) on hypoglycemic-hypoxic injury in hippocampal slices of rats. Methods Extracellular recording technique was used to record the peak potentials of CAl1 region in isolated hippocampal slices of rats. The duration of peak potentials (PS) and the degree of recovery were used as the standard of efficacy. Results The duration of PS in the control group and dihydropalmatine group was 335.13 ± 74.73s and 76.5 ± 2.66 8.30s respectively, which showed that the duration of PS in the DL group was significantly prolonged after hypoglycemia and hypoxia (compared with the control group, P <0. 05), while prazosin had no effect at 1 × 10 -6 mol·L-1. After 7 minutes and 30 seconds of hypoglycemia and hypoxia, the amplitude of PS in the control group was 4.93% ± 7.78%, while the DL (1 × 10 -6mol·L-1) group remained 48.2 ± 2 7.08%; compared with the control group, PS recovery in the group of 10mol DL (1 × 10-6mol·L-1 and 1 × 10-5mol·L-1) (1 × 10-6mol·L-1), DL (1 × 10-5mol·L-1), and phentolamine (5 × 10 ^ -5mol·L-1), PS returned to 14.17% ± 34.7%, 94.30% ± 49.10%, 71.0% ± 41.40%, 71.40% ± 46.0% before hypoglycemia and hypoxia, respectively. Conclusion DL can significantly protect hippocampal slices from hypoxia and hypoxia injury. The mechanism may be for the DL block adrenergic receptors and improve energy metabolism, thereby enhancing the ability of hippocampal slices against oxygen-glucose deprivation injury.