人参皂苷Rb1对癫痫大鼠海马组织线粒体的保护作用和机制探讨

Effects of ginsenoside Rb1 on mitochondrial damages of hippocampus in epileptic rats and related mechanism

目的探讨人参皂苷Rb1对戌四氮(PTZ)致痫大鼠海马线粒体结构和功能的作用及机制。方法采用PTZ 40mg·kg^(-1)·d^(-1)腹腔注射制备癫痫动物模型,绐予人参皂苷Rb1低剂量20mg·kg^(-1)·d^(-1)和高剂量80mg·kg^(-1)·d^(-1)连续干预30d后,分别检测海马组织中细胞内活性氧(ROS)和线粒体膜电位(△Ψm)的水平,MDA和SOD的含量,及胞质中Cytochrome c和Caspase3的表达,并观察海马CA1区线粒体的超微结构。结果与对照组相比,模型组大鼠海马中ROS水平升高,△Ψm水平降低(P<0.01);MDA含量升高,SOD活性减低(P<0.01),胞质中Cytochrome c和Caspase3的表达亦相应增加(P<0.05),且线粒体结构明显空泡化;而人参皂苷Rb1干预组剂量依赖性逆转了上述指标的异常改变。结论人参皂苷Rb1可挽救致痫大鼠海马组织中线粒体继发损伤,其机制可能与抗氧化、抗凋亡有关。

Objective To explore the effects of ginsenoside Rbl on mitochondrial damages of hippocampus in pentylenetetrazol（PTZ）-induced epileptic rats and related mechanism.Methods Rats were given PTZ40mg·kg^（-1）·d^（-1） and ginsenoside Rb1 20mg·kg^（-1）·d^（-1） and 80mg·kg^（-1）·d^（-1）.After 30 days,levels of reactive oxygen species（ROS） and mitochondrial membrane potential（△Ψm）,and levels of MDA and SOD were determined,respectively.Meanwhile,expressions of Cytochrome c and Caspase3 in the hippocampus cytoplasm were detected.What＇s more,mitochondrial ultrastructures were observed by electron microscope.Rseults Compared to the control group,increased ROS and decreased △Ψm（P0.01）,and increased MDA and decreased SOD（P0.01）were indicated in the PTZ group.Meanwhile,increased expressions of Cytochrome c and Caspase3（P0.05） and Objective To explore the effects of ginsenoside Rb1 on mitochondrial damages of hippocampus in pentylenetetrazol（ PTZ）-induced epileptic rats and related mechanism. Methods Rats were given PTZ40mg·kg-1·d-1and ginsenoside Rb1 20mg·kg-1·d-1and 80mg·kg-1·d-1. After 30 days,levels of reactive oxygen species（ ROS） and mitochondrial membrane potential（ ΔΨm）, and levels of MDA and SOD were determined,respectively. Meanwhile,expressions of Cytochrome c and Caspase3 in the hippocampus cytoplasm were detected.What＇s more,mitochondrial ultrastructures were observed by electron microscope. Rseults Compared to the control group,increased ROS and decreased ΔΨm（ P0.01）,and increased MDA and decreased SOD（ P0.01）were indicated in the PTZ group. Meanwhile,increased expressions of Cytochrome c and Caspase3（ P〈0. 05） andobvious mitochondria vacuolations were also demonstrated in the PTZ group,while ginsenoside Rb1 could dosedependently reversed these changes. Conclusion Ginsenoside Rb1 could effectively prevent hippocampal mitochondria damages of epileptic rats,which might be relevant to its anti-oxidative stress and anti-apoptosis properties.