摘要
目的研究甘草多糖对戊四氮点燃癫痫大鼠的影响及机制。方法通过戊四氮点燃构建癫痫大鼠模型,另取10只大鼠为对照组注射等量生理盐水。将癫痫大鼠随机分为模型组(n=20)及实验组(n=20)。实验组大鼠于戊四氮注射前1 h腹腔注射甘草多糖溶液(50 mg·kg-1),对照组和模型组注射等量生理盐水,连续干预30 d。以苏木精-伊红染色法观察海马神经元病理损伤,以酶联免疫吸附法检测各组大鼠海马组织氧化应激及炎性因子指标水平,以蛋白质印迹法检测各组海马组织细胞P2X7受体、核因子-κB(NF-κB)蛋白表达情况。结果模型组及实验组癫痫潜伏期分别为(14.35±2.61),(29.85±2.34)min,癫痫总持续时间分别为(34.52±7.58),(14.35±3.23)min。对照组、模型组及实验组大鼠海马组织坏死神经元数量分别为0,(18.32±2.63)和(6.58±3.05)个,P2X7受体蛋白表达量分别为0.15±0.03,1.22±0.36和0.35±0.06,NF-κB蛋白表达量分别为0.40±0.03,1.19±0.11,0.72±0.12,模型组分别与实验组及对照组比较,差异均有统计学意义(均P<0.05)。与对照组比较,模型组和实验组大鼠海马组织SOD降低,MDA及IL-18、TNF-α含量升高,其中实验组海马组织SOD高于模型组,MDA及IL-18、TNF-α含量低于模型组(均P<0.05)。结论甘草多糖可有效抑制戊四氮点燃癫痫大鼠氧化应激及炎性反应,减轻神经病理损伤程度,其作用机制可能与下调海马组织P2X7受体、NF-κB蛋白表达相关。
Objective To explore the effect and mechanism of glycyrrhiza polysaccharide on pentylenetetrazol kindled epileptic rats.Methods Epileptic rat model was established by pentylenetetrazol kindling.Another 10 rats were taken as control group and injected with the same amount of normal saline.Epilepsy rats were randomly divided into model group(n=20) and test group(n=20).Rats in test group were intraperitoneally injected with 50 mg·kg-1 glycyrrhiza polysaccharide solution one hour before pentylenetetranitrogen injection, rats in control group and model group were injected with the same amount of normal saline for 30 d.Hematoxylin eosin staining was used to observe the pathological damage of hippocampal neurons, enzyme-linked immunosorbent assay was used to detect the levels of oxidative stress and inflammatory factors in hippocampal tissues of rats in each group, and Western blotting was used to detect the expression of P2 X7 receptor and nuclear factor-κB(NF-κB) in hippocampal cells of each group.Results The latency period of epilepsy in model group and test group were(14.35 ± 2.61) and(29.85 ± 2.34)min,the total duration of epilepsy were(34.52 ± 7.58) and(14.35 ± 3.23) min.The number of necrotic neurons in control group,model group and test group were 0,18.32 ± 2.63 and 6.58 ± 3.05,the expression of P2 X7 receptor protein were 0.15 ± 0.03,1.22 ± 0.36 and 0.35 ± 0.06,the expression of NF-κB protein were 0.40 ± 0.03,1.19 ± 0.11 and 0.72 ± 0.12,the difference which in model group were all with statistically significant compared with test group and control group(all P < 0.05).Compared with control group,the SOD of hippocampus in model group and test group were decreased,and the content of MDA and IL-18,TNF-α were increased,the SOD of hippocampus in test group was higher than that in model group,the content of MDA and IL-18,TNF-α were lower than those in model group(all P < 0.05).Conclusion Glycyrrhiza polysaccharide can effectively inhibit oxidative stress and inflammatory response in pentylenetetrazol kindled epileptic rats,and reduce the degree of neuropathological damage.The mechanism may be related to the down-regulation of P2 X7 receptor and NF-κB protein expression in hippocampus.
作者
肖剑辉
王琴
刘作良
XIAO Jian-hui;WANG Qin;LIU Zuo-liang(Department of Emergency,Guangzhou Medical University Affiliated Shenzhen Shaijing Hospital,Shenzhen 518040,Guangdong Province,China;Department of Infection,Xiangya Hospital,Central South University,Changsha 410013,Hunan Province,China;Department of Critical Care Medicine,Xiangya Third Hospital,Central South University,Changsha 410013,Hunan Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2021年第4期432-435,共4页
The Chinese Journal of Clinical Pharmacology
关键词
癫痫
甘草多糖
氧化应激
P2X7受体
核因子-ΚB
炎性反应
epilepsy
glycyrrhiza polysaccharide
oxidative stress
P2X7 receptor
nuclear factorκB
inflammatory response
