首页|小白菊内酯对杏仁核电点燃大鼠的神经保护作用及机制

小白菊内酯对杏仁核电点燃大鼠的神经保护作用及机制

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目的 探讨小白菊内酯对杏仁核电点燃癫痫大鼠行为学影响及其机制.方法 将40 只雄性SD大鼠随机分为4 组,每组10 只.对照组不进行电刺激,每天给予Tween80 腹腔注射;模型组、小白菊内酯低剂量组、小白菊内酯高剂量组每天给予1 次电刺激制备杏仁核电点燃癫痫模型,其中小白菊内酯低、高剂量组于电刺激1h前分别给予小白菊内酯250 μg/kg、500 μg/kg腹腔注射,模型组给予Tween80 腹腔注射,共干预15 d.观察各组大鼠癫痫发作情况;电刺激结束后24h行Morris水迷宫实验,记录大鼠逃避潜伏期及穿越平台象限百分比;然后检测脑组织中丙二醛(MDA)和还原型谷胱甘肽(GSH)含量,透射电镜观察海马CA1 区超微结构.结果 随着造模时间的延长,癫痫造模各组大鼠癫痫发作等级逐渐升高,但小白菊内酯低、高剂量组大鼠癫痫发作级别均明显低于模型组(P均<0.05),且小白菊内酯高剂量组明显低于同期小白菊内酯低剂量组(P均<0.05).水迷宫实验中,模型组大鼠第1~4 天的逃避潜伏期均明显长于对照组(P均<0.05),穿越平台象限百分比明显低于对照组(P<0.05);小白菊内酯低、高剂量组大鼠第 1~4 天的逃避潜伏期均明显短于模型组(P均<0.05),穿越平台象限百分比均明显高于模型组(P均<0.05);可视平台实验中,各组大鼠逃避潜伏期、游泳速度比较差异均无统计学意义(P均>0.05).与对照组比较,模型组大鼠脑组织中MDA含量明显升高(P<0.05),GSH含量明显降低(P<0.05);海马突触间隙明显增宽(P<0.05),活性带长度明显缩短(P<0.05),突触后致密物厚度明显降低(P<0.05).与模型组比较,小白菊内酯低、高剂量组大鼠MDA含量均明显降低(P均<0.05),GSH含量均明显升高(P均<0.05);海马突触间隙均明显缩短(P均<0.05),活性带长度均明显变长(P均<0.05),突触后致密物厚度均明显增加(P均<0.05).与小白菊内酯低剂量组比较,小白菊内酯高剂量组大鼠脑组织中MDA、GSH含量变化更明显(P均<0.05).结论 小白菊内酯对杏仁核癫痫大鼠有很好的神经保护作用,机制可能与其抗氧化和保护海马超微结构有关.
Parthenolide protects nerves of rats with epilepsy induced by amygdale electrical ignition and its mechanism
Objective It is to investigate the effects of parthenolide(PTL)on the behavior of rats with epilepsy in-duced by amygdale electrical ignition and its mechanism.Methods Forty male SD rats were randomly divided into 4 groups,with 10 rats in each group.The control group was not electrically stimulated,and was given Tween80 by intraper-itoneal injection every day;the model group,the PTL low-dose group and PTL high-dose group were given once of electrical stimulation every day to prepare the models of amygdala electrical ignition epilepsy,the PTL low-dose group and PTL high-dose groups were given 250 μg/kg and 500 μg/kg of PTL by intraperitoneal injections at 1 h before the electrical stimula-tion,respectively,and the model group was given Tween80 by intraperitoneal injection,totally treated for 15 days.The ep-ileptic seizures of rats in each group were observed;the rats were tested by Morris water maze test at 24 h after electrical stimulation finished,and their escape latency and the percentage of crossing the platform quadrant were recorded;then,the contents of malondialdehyde(MDA)and reduced glutathione(GSH)in cerebral tissue were detected,and the ultrastruc-ture of hippocampal CA1 was observed by transmission electron microscopy.Results With the extension of modeling time,the epileptic seizure classification of rats in each epilepsy modeling group were gradually increased,but the epileptic seizure classification of rats in both the low and high dose groups of PTL was significantly lower than that of the model group(both P<0.05),and the high dose group was significantly lower than the low dose group at the same period(all P<0.05).In the water maze test,the escape latency of rats in the model group was significantly longer than that of the control group from day 1 to 4(all P<0.05),and the percentage of crossing the platform quadrant was significantly lower than that of the con-trol group(all P<0.05);the escape latency of rats in both the low and high dosage groups of PTL was significantly shorter than that of the model group(both P<0.05),and the percentage of crossing the platform quadrant was significantly higher than that of the model group(all P<0.05);in the visual platform test,the differences in the escape latency and swimming speed of rats were not statistically significant among each group(all P>0.05).Compared with the control group,the con-tent of MDA in cerebral tissue of rats were significantly increased while the content of GSH was significantly decreased in the model group(both P<0.05);the hippocampal synaptic gap was significantly widened(P<0.05),the length of the active band was significantly shortened(P<0.05),and the postsynaptic density was significantly reduced(P<0.05).Compared with the model group,the contents of MDA in cerebral tissue of rats were significantly decreased while the con-tents of GSH were significantly increased in both the low and high dose groups of PTL(all P<0.05);the hippocampal synaptic gaps were significantly reduced(both P<0.05),the lengths of the active band were significantly lengthened(both P<0.05),and the postsynaptic densities were significantly increased(both P<0.05).The changes of MDA and GSH contents in cerebral tissues of rats in the PTL high-dose group were more than those in the PTL low-dose group(both P<0.05).Conclusion Parthenolide has a good neuroprotective effect on amygdala epilepsy rats,and its mechanism may be related to its antioxidant effect and neuroprotection of hippocampus ultrastructure.

epilepsyparthenolideoxidative stressultrastructure of hippocampus

谢涛、和学欣、孙倩、毛卓锋、王晓鹏

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河北医科大学第二医院,河北 石家庄 050000

石家庄市中医院,河北 石家庄 050000

癫痫 小白菊内酯 氧化应激 海马超微结构

国家自然科学基金河北省中医药局科研项目

816712922023326

2024

现代中西医结合杂志
中国中西医结合学会河北分会,中华中医药学会

现代中西医结合杂志

CSTPCD
影响因子:1.775
ISSN:1008-8849
年,卷(期):2024.33(7)
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