天麻对铅所致大鼠海马损害的拮抗作用

目的　观察并探讨天麻对铅所致学习记忆损害的拮抗作用。方法　选用 36只Wistar大鼠 ,随机分为 3组 ,每组 12只。 (1)对照组 :给予蒸馏水 ;(2 )染铅组 :醋酸铅 (0 .1g·kg-1·d-1) ;(3)天麻铅组 :醋酸铅 (0 .1g·kg-1·d-1) +天麻 (4.0g·kg-1·d-1)。每月用游泳试验测试学习记忆 1次。 3个月后处死大鼠 ,分别测定大鼠海马一氧化氮 (NO)和总抗氧化能力 (TAOC)并进行病理检查。结果　 (1)在游泳试验中 ,染铅组大鼠 5min内到达平台次数 (1、2、3月分别为 :10 .1± 1.10、7.8± 1.30、5 .4±0 .97)低于对照组 ,差异有显著性 (P <0 .0 1) ;天麻铅组大鼠到达平台的次数 (1、2、3月分别为 :11.9±0 .95、10 .9± 0 .95、9.7± 0 .96 )高于染铅组 ,差异有显著性 (P <0 .0 1)。 (2 )染铅组大鼠海马NO含量为(0 .733± 0 .0 15 ) μmol/gpro和TAOC为 (0 .94 5± 0 .0 17)U/mgpro ,低于对照组 ,差异有显著性 (P <0 .0 1) ;天麻铅组海马NO含量为 (0 .76 9± 0 .0 2 1) μmol/gpro和TAOC为 (0 .986± 0 .0 10 )U/mgpro ,高于染铅组 ,差异有显著性 (P <0 .0 1)。 (3)病理检查 :染铅组大鼠海马明显萎缩 ,细胞变性坏死、脱失明显 ,轴突溶解或消失 ;天麻铅组海马萎缩不明显 ,细胞形态基本正常 ,无明显坏死、脱失现象 ,轴

The antagonism of rhizoma gastrodiae to lead-induced damage of hippocampus in rats

OBJECTIVE: To observe and explore the antagonism of rhizoma gastrodiae (RGT) to the impairment of learning and memory ability induced by lead in rats. METHODS: 36 Wistar rats were randomly divided into 3 groups, 12 rats in every group, (1) control group: treated with distilled water; (2) lead group: treated with lead acetate (0.1 g.kg-1.d-1); (3) lead-RGT group: lead acetate (0.1 g.kg-1.d-1) + RGT(4.0 g.kg-1.d-1). The ability of learning and memory of the rats was measured monthly by swimming test; 3 months later, the rats were decapitated and nitric oxide(NO) and total antioxidative capacity(TAOC) in hippocampus were measured immediately and the examination for pathology was also made. RESULTS: (1) In swimming test, the number of seeking for anchorage in lead group(1, 2, 3 month: 10.10 +/- 1.10, 7.80 +/- 1.32, 5.40 +/- 0.97 respectively) were significantly decreased, compared with the control(P < 0.01); the number of seeking for anchorage in RGT-lead group(1, 2, 3 month: 11.90 +/- 0.95, 10.90 +/- 0.95, 9.70 +/- 0.96 respectively) were significantly increased, compared with lead group(P < 0.01). (2) NO (0.733 +/- 0.015) mumol/g pro and TAOC (0.945 +/- 0.017) U/mg pro in hippocampus of lead group were significantly decreased compared with the control(P < 0.01) whereas NO(0.769 +/- 0.021) mumol/g pro and TAOC(0.986 +/- 0.010) U/mg pro in hippocampus of RGT-lead group were significantly increased compared with lead group(P < 0.01). (3) Pathological examination showed that in lead group, marked atrophy in hippocampus, cellular denaturation and necrosis, dissolution and disappearance in axon were found. In lead-RGT group, the atrophy of hippocampus was not obvious, the cell morphology was nearly normal, no obvious abnormal changes were seen. CONCLUSION: RGT is antagonistic to the impairment of hippocampus and of learning and memory ability induced by lead.