摘要
目的:研究间歇低氧对幼鼠纹状体边缘区p38MAPK及超微结构的影响及芹菜素的干预作用。方法:SPF级健康雄性SD幼鼠(3~4周龄)40只,随机分为4组:间歇低氧2周组(IH组)、对照组(C组)、芹菜素+二甲基亚砜组(Q组)和二甲基亚砜组(R组)。建立间歇低氧幼鼠模型,以RT-PCR法和Westernblot法分别测幼鼠纹状体内侧边缘区p38MAPK mRNA和磷酸化p38MAPK(p-p38)蛋白的表达,并电镜观察超微结构的改变。结果:IH组幼鼠纹状体边缘区的p38MAPK mRNA及p-p38蛋白均明显高于C组(P均<0.01),Q组的表达则明显低于R组(P均<0.01),电镜下IH组和R组纹状体边缘区组织细胞核膜模糊不清晰,染色质浓缩、边聚,线粒体肿胀空泡化,Q组和C组无明显变化。结论:间歇低氧可激活幼鼠脑区p38MAPK,进而引起超微结构的改变,而芹菜素可至少部分抑制这种激活,这可能对减轻间歇低氧后纹状体边缘区等脑区损伤具有积极意义。
Objective:To explore the infusion of intermittent hypoxia on p38MAPK and ultrastructure changes in marginal striatum of weanling rats and the intervention effects of apigenin.Methods:Randomly,fourty male Sprague-Dawley rats(3-week.old^4-week-old)were divided into four groups:2-weeek-IH group(IH),control group(C),apigenin+DMSO(Q)group and DMSO control(R)group.Intermittent hypoxia model was induced by an intermittent hypoxia cabin.In medial border of the striatum,the marginal division(MrD),the expression of p38MAPK mRNA and the phosphorylation levels of p38MAPK(phospho-p38)were measured by RT-PCR or Westernblot respectively.The ultrastructure of MrD was studied by electron microscope.Results:In the MrD,the expression of p38MAPK mRNA and p-p3 8 protein in IH group were respectively higher than C group(P〈0.01,respectively).These expressions in Q group had significantly less than in R group(P〈0.01,respectively).The nuclear membrane of MrD cells in IH or R groups were broken,chromatin concintration and edge accumulation and some mitochondria were enlarged and vacuoled.Conclusions:Intermittent hypoxia actived the p38MAPK signal transduction,led ultrastructure of neuron disordered in brain regions.Apigenin can partial reduce the activation of p38MAPK which may play a positive role in alleviating the cerebral tissues injury in intermittent hypoxia weanling rats.
出处
《中华中医药学刊》
CAS
2008年第12期2615-2618,共4页
Chinese Archives of Traditional Chinese Medicine
基金
浙江省医药卫生科学研究基金项目(20068104)
浙江省科技厅新苗人才计划项目(2007G60G2090029)
温州市科技局基金资助项目(Y2006A007)
关键词
间歇低氧
P38丝裂原活化蛋白激酶
纹状体
芹菜素
Intermittent hypoxia
p38-mitogen-activatedprotein kinases
Striatum
Marginal division
Apigenin