摘要目的 观察双参提取物对慢性脑低灌注大鼠海马神经元的保护作用,并从星形胶质细胞活化和DNA修复蛋白表达方面探讨其作用机制.方法 采用随机数字表法将50只SD雄性大鼠随机分为假手术组,模型组,双参提取物小、大剂量组,金纳多组,每组10只.除假手术组外,其余各组大鼠制备双侧颈总动脉永久性结扎模型.造模后24 h开始给药,双参提取物小、大剂量组分别灌胃双参提取物溶液2.2、4.4 g/kg,金纳多组灌胃金纳多溶液60 mg/kg,假手术组及模型组灌胃等体积生理盐水.1次/d,连续给药30 d.末次给药后,采用免疫荧光染色结合图像分析技术检测各组大鼠海马区神经元核抗原(neuronal nuclei,NeuN)、胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)及腺苷二磷酸核糖聚合酶(poly adenosinediphosphate-ribose polymerase,PARP)的表达.结果 与模型组比较,双参提取物小、大剂量组大鼠海马NeuN表达[(206.39±11.91)、(222.89±12.27)比(129.87±21.62)]、GFAP表达[(263.48±32.70)、(293.27±20.25)比(187.52±19.20)]升高(P<0.05),PARP表达[(771.44±55.03)、(718.61±58.43)比(1056.56±45.56)]降低(P<0.05).结论 双参提取物可减轻慢性脑低灌注致海马神经元损伤,其作用可能与促进星形胶质细胞适度活化、降低PARP过度表达有关.

abstractsObjective To observe the regulation ofShuangshen extract on the NeuN, GFAP and PARP expression for the mechanism.Methods The male SD rats were randomly divided into the sham-operation group, the model group, the low dose group, the large dose group and ginaton group by random digits table, 10 rats per group. In addition to the sham operation group, other groups prepared permanent carotid artery occlusion model in rats. The low dose group and large dose group were orally givenShuangshen extract, respectively, with 2.2 and 4.4 g/kg; the ginaton group was orally given ginalton with 60 mg/kg and the sham-operation group and model group were given equal volume of saline. All the interventions were once per day and continued 30 days. At the last day of drugs, the expressions of NeuN, GFAP and PARP were detected by using immunofluorescence staining combined image analysis technique.Results Compared with the model group, the fluorescence intension of NeuN (206.39 ± 11.91, 222.89 ± 12.27vs. 129.87 ± 21.62) and GFAP (263.48 ± 32.70, 293.27 ± 20.25vs. 187.52 ± 19.20) in theShuangshen extractive low dose group and large dose group significantly increased (P<0.05), while the fluorescence intension of PARP (771.44 ± 55.03, 718.61 ± 58.43vs.1056.56 ± 45.56) significantly decreased (P<0.05).Conclusions TheShuangshen extract showed its protective effect on the neurons in ischemic brain tissues of hippocampus through the mechanism of activating the NeuN and GFAP while decreased the over-expression of PARP.