熟地黄对ADHD模型大鼠前额叶皮质线粒体的保护作用

目的探讨熟地黄对ADHD模型大鼠前额叶皮质线粒体保护作用。方法将30只SHR大鼠随机分为模型组、MPH组(2 mg/kg)、熟地黄组(2.4 g/kg),另设WKY大鼠为正常组,每组10只,灌胃给药4周。采用透射电镜观察大鼠前额叶皮质线粒体超微结构;JC-1染色法和DCFH-DA荧光探针分别检测线粒体膜电位(MMP)和细胞内活性氧簇(ROS)水平;比色法检测超SOD、CAT水平;TUNEL染色检测神经元凋亡。结果与正常组比较,模型组线粒体呈现出肿胀、嵴减少等异常,MPH组上述异常加重,熟地黄组则有所缓解。与模型组比较,MPH组前额叶皮质MMP、SOD水平降低(P<0.05,P<0.01),ROS水平及神经元凋亡升高(P<0.05,P<0.01);而熟地黄组前额叶皮质MMP及SOD、CAT水平升高(P<0.05,P<0.01),ROS水平及神经元凋亡降低(P<0.01)。结论熟地黄对ADHD模型SHR前额叶皮质线粒体结构和功能损伤有保护作用,并可减少神经元凋亡,其机制可能与抗氧化应激损伤有关。

Protective effects of Rehmanniae Radix Preparata on prefrontal cortex mitochondria of ADHD model rats

AIM To investigate the protective effects of Rehmanniae Radix Preparata(RRP)on prefrontal cortex mitochondria of ADHD model rats.METHODS Thirty SHR were randomly divided into model group,methylphenidate(MPH)group(2 mg/kg),RRP group(2.4 g/kg),ten rats in each group;and another ten WKY rats were assigned into the normal group,upon whom corresponding 4 weeks gavage administration was applied respectively.The rats were subjected to the observation of the mitochondria ultrastructure by transmission electron microscopy,the detection of mitochondrial membrane potential(MMP)and reactive oxygen species(ROS)level by JC-1 staining and DCFH-DA fluorescence probe respectively,the measurement of levels of superoxide SOD and CAT by colorimetry,and the detection of neuronal apoptosis by TUNEL staining.RESULTS Compared with the normal group,the model group showed mitochondrial abnormalities,including swelling and cristae reduction,while MPH group presented with even aggravated condition,and the RRP group displayed alleviated condition.Compared with the model group,the MPH group shared decreased MMP and SOD levels in the prefrontal cortex(P<0.05,P<0.01),increased ROS levels and neuronal apoptosis(P<0.05,P<0.01);the RRP group demonstrated increased levels of MMP,SOD and CAT(P<0.05,P<0.01),and decreased ROS levels and neuronal apoptosis(P<0.01).CONCLUSION RRP can protect the structure and function of prefrontal cortex mitochondria of young SHR,and inhibit their neuronal apoptosis,probably through reducing oxidative stress injury.