茯苓多糖对癫痫大鼠海马神经细胞凋亡及Nrf2ARE信号通路的影响  

Effects of poria cocos polysaccharide on hippocampal neural apoptosis and Nrf2ARE signaling pathway in epileptic rats

作　　者：梁静[1] 陈汉仁 毛敏芸 蒋静子[1] 彭天婵 LIANG Jing;CHEN Hanren;MAO Minyun(Department of Neurology,Affiliated Hospital of Guilin Medical University,Guangxi,Guilin 541001,China)

机构地区：[1]桂林医学院附属医院神经内科,广西壮族自治区桂林市541001

出　　处：《河北医药》2023年第2期194-197,共4页Hebei Medical Journal

摘　　要：目的 探讨茯苓多糖(PPC)对癫痫大鼠海马神经细胞凋亡的影响及可能的作用机制。方法 将SD大鼠分为NC组、Model组、茯苓多糖、中、高低剂量组(PPC-L组,50 mg/kg;PPC-M组,100 mg/kg;PPC-H组,200 mg/kg),每组12只。除NC组外,其他组均需构建癫痫大鼠模型。建模成功后,给药处理,1次/d,连续14 d。比较5组大鼠癫痫发作潜伏期的差异;通过Morris水迷宫实验检测各组大鼠逃避潜伏期、穿越平台次数;超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、还原型谷胱甘肽(GSH)试剂盒分别检测海马组织中CAT、SOD、GSH水平;TUNEL染色检测神经细胞凋亡;western blot检测大鼠海马组织中活化的Caspase-3(Cleaved-Caspase-3)、Bax、核因子E2相关因子2 (Nrf2)、血红素氧化酶(HO-1)、醌氧化还原酶1(NQO-1)蛋白表达。结果 与NC组比较,Model组大鼠逃避潜伏期延长,穿越平台次数减少,海马组织中SOD、CAT、GSH水平及Nrf2、HO-1、NQO-1蛋白表达水平显著降低,神经细胞凋亡率、Cleaved-Caspase-3、Bax蛋白表达水平显著升高(P<0.05);与Model组比较,PPC-L组、PPC-M组、PPC-H组大鼠癫痫发作潜伏期延长,逃避潜伏期缩短,穿越平台次数增加,海马组织中SOD、CAT、GSH水平及Nrf2、HO-1、NQO-1蛋白表达明显升高,神经细胞凋亡率、Bax、Cleaved-Caspase-3蛋白表达明显降低(P<0.05)。结论 PPC可抑制氧化应激,减少神经细胞凋亡,发挥抗癫痫作用,该机制可能与激活Nrf2/ARE信号通路有关。Objective To explore the effects of poria cocos polysaccharide(PCP) on hippocampal neural apoptosis in epileptic rats and possible mechanism.Methods The SD rats were assigned to the normal control(NC) group,model group,PCP low-dose group(PCP-L group,50mg/kg),PCP medium-dose group(PCP-M group,100mg/kg) and PCP high-dose group(PCP-H group,200mg/kg) with 12 rats per group.The epileptic rat models were established in the other groups except for NC group.The dosing regimen based on once daily for 14 days following successful modeling.The differences of seizure latency between groups were compared,Morris water maze(MWM) was used to detect escape latency,the number of cross-platform.The test kits were conducted to analyze for superoxide dismutase(SOD),catalase(CAT) and glutathione(GSH).The hippocampal neural apoptosis was observed by TUNEL staining.Western blot was porformed to assess the protein expression of cleaved caspase-3,Bcl-2 associated X protein(Bax),nuclear factor E2-related factor 2(Nrf2),heme oxygenase-1(HO-1) and quinone oxidoreductase 1(NQO1) in hippocampus organization.Results Prolonged escape latency and decreased crossing-platform were found in model group as compared to in NC group;the level of SOD,CAT,GSH and the protein expression of Nrf2,HO-1 and NQO1 in model group were significantly decreased than those in NC group,while the rate of neuronal apoptosis,cleaved-caspase-3,Bax expression in model group were evidently increased(P<0.05).Compared with model group,the seizure latency in PCP-L,PCP-M and PCP-H groups was prolonged,the escape latency was shortened,crossing-platform frequency increased,the level of SOD,CAT,GSH and the protein expression of Nrf2,HO-1 and NQO1 were notably elevated,the rate of neuronal apoptosis,cleaved-caspase-3 and Bax expression were obviously decreased(P<0.05).Conclusion PCP functionalizes anti-epileptic effect by inhibiting the oxidative stress and reducing neuronal apoptosis,and the mechanism may be related to the activated Nrf2/ARE signaling pathway.

关 键 词：茯苓多糖 癫痫 氧化应激 细胞凋亡 

分 类 号：R742.1[医药卫生—神经病学与精神病学]