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目的探讨人参皂甙RD对大鼠蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后脑血管痉挛(cerebral vasospasm,CVS)的防治作用及作用机制。方法 48只SD大鼠随机分为穿刺组、模型组、人参皂苷RD组和丙二醇组,每组12只;模型组、人参皂苷RD组和丙二醇组采用枕大池二次注血法建立大鼠SAH模型,穿刺组仅行枕大池穿刺而不注血,模型组造模后无干预措施,人参皂苷RD组和丙二醇组造模后分别腹腔注射人参皂甙RD稀释液和丙二醇,1次/d;造模5d后行神经行为学评分,采用HE染色和透射电镜观察基底动脉形态和超微结构改变。结果人参皂苷RD组神经行为学评分(3.75±0.62)明显高于模型组(3.17±0.72)和丙二醇组(3.25±0.45),低于穿刺组(4.92±0.29)(P<0.05);人参皂苷RD组基底动脉管壁厚度((20.03±0.44)μm)明显小于模型组((25.12±0.37)μm)和丙二醇组((25.06±0.38)μm),大于穿刺组((16.89±0.41)μm)(P<0.05),管腔面积((36.39±1.41)×103μm2)明显大于模型组((21.20±0.86)×103μm2)和丙二醇组((21.41±1.03)×103μm2),小于穿刺组((55.09±1.20)×103μm2)(P<0.05);人参皂苷RD组基底动脉超微结构病理性改变减轻。结论非电压依赖性钙通道拮抗剂人参皂甙RD可在一定程度上缓解CVS。
Objective To investigate the preventive and therapeutic effects of ginsenoside RD on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in rats and its mechanism. Methods 48 Sprague-Dawley rats were randomly divided into puncture group, model group, ginsenoside RD group and propylene glycol group, with 12 rats in each group. The model group, the ginsenoside RD group and the propylene glycol group were used to establish SAH Model, the puncture group only puncture the big pool puncture without injection of blood, the model group no intervention after modeling, ginsenoside RD group and propylene glycol group were injected intraperitoneal injection of ginsenoside RD and propylene glycol, 1 / d; The model of neurobehavioral score was performed 5 days later. Morphological and ultrastructural changes of the basilar artery were observed by HE staining and transmission electron microscopy. Results The neurobehavioral score (3.75 ± 0.62) of ginsenoside RD group was significantly higher than that of model group (3.17 ± 0.72) and propylene glycol group (3.25 ± 0.45), lower than that of puncture group (4.92 ± 0.29) (P <0.05) The thickness of basilar artery wall in RD group was (20.03 ± 0.44) μm less than that in the model group (25.12 ± 0.37 μm) and propanediol group (25.06 ± 0.38 μm), significantly higher than that in the puncture group (16.89 ± 0.41 μm) (P <0.05). The lumen area was (36.39 ± 1.41) × 103μm2) was significantly larger than that in the model group (21.20 ± 0.86) × 103μm2 and the propylene glycol group (21.41 ± 1.03 × 103μm2) ± 1.20) × 103μm2) (P <0.05). The pathological changes of basilar artery in ginsenoside RD group were alleviated. Conclusion Ginsenoside RD, a non-voltage-dependent calcium channel antagonist, can relieve CVS to some extent.