摘要
目的 研究氟美松对成年大鼠局灶性脑缺血后细胞凋亡及相关Fas基因表达的作用。方法 健康雄性SD大鼠随机分成 14组 (每组 5只 )。 1～ 7组为对照组 ,8～ 14组为实验组。用右侧近端大脑中动脉电凝术建立大鼠持续性局灶性脑缺血模型。缺血后 1h ,实验组动物尾静脉注射氟美松(5mg/kg) ,对照组注射生理盐水。分别在缺血后 3、6、12、2 4、48、72和 12 0h取材 ,用原位末端标记(TUNEL法 )、原位RT PCR法分别检测缺血后细胞凋亡和FasmRNA表达并进行了半定量分析。结果 氟美松可导致缺血后细胞凋亡提前发生 ,促进大鼠局灶性脑缺血后FasmRNA的表达 ,使其表达开始时间提前、表达持续时间延长、表达细胞增多及表达信号增强。结论 氟美松可促进缺血后细胞凋亡相关基因FasmRNA的表达 ,可能是其加重成年大鼠缺血性脑损伤尤其是缺血后细胞凋亡的机制之一。
Objective To investigate the possible role and mechanism of the neurotoxic effect of dexamethasone on adult rats after having focal cerebral ischemia. Methods The rat model of focal cerebral ischemia was established by permanent middle cerebral artery occlusion (MCAO) One hour after ishemia,the experimental groups were treated with dexamethasone (5 mg/kg) while the control groups were treated with saline TUNEL staining and In-suit RT-PCR were used to show the changes of apoptosis and the expression of Fas mRNA at ipsilateral cerebral hemisphere. Results TUNEL positive cells were present in a time from 48 h to 72 h, localizing at peripheral ischemic area The expression of Fas mRNA at peripheral ischemic area in control groups began at 12 h, peaked at 24 h, and decreased to a lower level at 48 h and 72 h, and returned to the baseline at 120 h Treatment with dexamethasone after ischemia made apoptosis present at 24 h and the number of TUNEL positive cells at 48 h exceeded that in the control group at 48 h ( P <0 01) Dexamethasone also induced an early expression of Fas mRNA at 6 h,increased at 12 h, peaked at 24 h,and continued at 48 h to 120 h. Conclusion After treatment of dexamethasone, the neuron apoptosis of adult rats may be aggravated in following permenant focal ischemia, which may be partially due to positive induction of the expression of Fas mRNA
出处
《中华神经科杂志》
CAS
CSCD
2000年第6期364-367,I032,共5页
Chinese Journal of Neurology
