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目的:观察脂多糖(LPS)对γ-丁内酯(GBL)诱导大鼠失神发作皮层脑电图棘慢波(SWDs)的影响,并推测其可能的机制。方法:40只SD大鼠随机分为4组:实验1、2、3组及对照组,每组10只。分别腹腔注射LPS50μg/kg、100μg/kg、200μg/kg及NS1ml,1h后每组随机取5只大鼠处死取海马用RT-PCR方法检测IL-1βmRNA表达的变化;另外5只大鼠腹腔注射GBL200mg/kg诱发失神发作,观察皮层脑电图(ECoG)SWDs潜伏时间、持续时间的改变。结果:LPS腹腔注射后1h大鼠海马组织IL-1βmRNA表达:50μg/kg组0.196±0.04、100μg/kg组0.285±0.057、200μg/kg组0.404±0.072,与对照组(0.131±0.034)比较均有显著差异(P<0.05);另外,LPS不同剂量组大鼠失神发作SWDs放电潜伏时间均较对照组缩短、持续时间延长,两者有显著差异(P<0.05)。其中实验2、3组SWDs潜伏时间与持续时间较实验1组潜伏时间更为缩短,持续时间更为延长(P<0.05);但实验3组SWDs潜伏时间和持续时间与实验2组比较没有差异(P>0.05)。结论:LPS能影响GBL诱导大鼠失神发作的SWDs发放,缩短其潜伏时间、延长持续时间,并且有剂量依赖性及饱和性,其机制可能与LPS刺激机体引起的免疫异常有关。
OBJECTIVE: To observe the effect of lipopolysaccharide (LPS) on spine and slow wave (SWDs) in cortical EEG induced by γ-butyrolactone (GBL) in rats and to speculate its possible mechanism. Methods: Forty SD rats were randomly divided into 4 groups: experimental group 1, group 2 and control group, with 10 in each group. The rats in each group were sacrificed and the hippocampus were sacrificed. The expression of IL-1βmRNA was detected by RT-PCR. Five rats were injected intraperitoneally with LPS 50μg / kg, 100μg / kg, 200μg / kg and NS1ml respectively. GBL200mg / kg induced seizures, observed cortical electroencephalogram (ECoG) SWDs latency, duration of change. Results: The expression of IL-1βmRNA in hippocampus of rats at 1 hour after intraperitoneal injection of LPS was 0.196 ± 0.04 in 50μg / kg group, 0.405 ± 0.057 in 200μg / kg group, 0.404 ± 0.072 in 200μg / kg group and 0.131 ± 0.034 in control group (P <0.05). In addition, the discharge latency of SWDs in rats with different doses of LPS was shorter and longer than that of the control group (P <0.05). The latency and duration of SWDs in experimental group 2 and 3 were shorter and longer than that in experimental group 1 (P <0.05), but the latency and duration of SWDs in experimental group 3 were not different from those in experimental group 2 (P> 0.05). CONCLUSION: LPS can affect the release of SWDs induced by GBL-induced absent seizures, shorten the latency and prolong the duration of LPS-induced SWDs in a dose-dependent and saturated manner in rats. The mechanism may be related to the abnormal immune response induced by LPS stimulation.