桑椹花青素-3-葡萄糖苷对癫痫模型小鼠的保护作用及海马BDNF/TrkB通路的影响
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篇名: 桑椹花青素-3-葡萄糖苷对癫痫模型小鼠的保护作用及海马BDNF/TrkB通路的影响
TITLE: Study on Protection Effect of Mulberry Anthocyanin- 3-glucoside on Epilepsy Model Mice and the Effect of Hippocampal BDNF/TrkB Pathway
摘要: 目的:研究桑椹花青素-3-葡萄糖苷对癫痫模型小鼠的保护作用及海马脑源性神经营养因子(BDNF)/酪氨酸激酶受体B(TrkB)通路的影响。方法:将120只C57BL/6小鼠随机分为正常组、模型组、单药(桑椹花青素-3-葡萄糖苷)和激动剂联用组(桑椹花青素-3-葡萄糖苷+TrkB激动剂LM22B-10),每组30只。单药组和激动剂联用组小鼠每天灌胃600μg/kg桑椹花青素-3-葡萄糖苷1次、连续给药6周,激动剂联用组小鼠在给药第6周时每天侧脑室注入LM22B-10(5mg/kg)1次;正常组和模型组小鼠灌胃等体积生理盐水。末次给药后,除正常组外,其余各组小鼠均采用氯化锂-匹罗卡品建立癫痫模型。造模成功后,各组分别取10只小鼠记录其癫痫自发性再发作的潜伏期、发作频率及持续时间,每天观察6h,连续观察4周;并于造模第14、28、36天记录其脑电图,统计1h内脑电波异常发生次数。于造模后第6天,各组分别取10只小鼠检测其血清钙离子水平,并取各组剩余10只小鼠检测其海马组织中BDNFmRNA及蛋白表达。结果:与正常组比较,模型组小鼠癫痫自发性再发作的潜伏期、发作频率、持续时间及造模第14、28、36天脑电波异常发生次数均显著增加(P<0.05),血清钙离子水平及海马BDNFmRNA、蛋白相对表达量均显著升高(P<0.05)。与模型组比较,单药组小鼠癫痫自发性再发作行为的潜伏期、发作频率、持续时间及造模第28、36天脑电波异常发生次数均显著减少(P<0.05),血清钙离子水平及海马BDNFmRNA、蛋白相对表达量均显著降低(P<0.05);与单药组比较,激动剂联用组小鼠癫痫自发性再发作的潜伏期、发作频率、持续时间及造模第28、36天脑电波异常发生次数均显著增加(P<0.05),血清钙离子水平及海马BDNFmRNA、蛋白相对表达量均显著升高(P<0.05)。结论:桑椹花青素-3-葡萄糖苷对癫痫模型小鼠具有一定的保护作用,其机制可能与抑制海马BDNF/TrkB通路的激活有关。
ABSTRACT: OBJECTIVE:To study the protection ef fects of mulberry anthocyanin- 3-glucoside on epilepsy model mice and the effect of hippocampal brain derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB)pathway. METHODS :Totally 120 C57BL/6 mice were randomly divided into normal group ,model group ,single medication group (mulberry anthocyanin- 3- glucoside),agonist combination group(mulberry anthocyanin- 3-glucoside+TrkB agonist LM 22B-10),with 30 mice in each group. single medication group and agonist combination group were given mulberry anthocyanin- 3-glucoside 600 μg/kg intragastrically once a day ,for consecutive 6 weeks. The agonist combination group was given LM22B-10(5 mg/kg)via the lateral ventricle once a day at 6th week. Normal group and model group were given constant volume of normal saline intragastrically. After last medication,except for normal group ,other groups were given lithium chloride-pilocarpine to establish epilepsy model. After modeling,10 mice in each group were taken to record the latency ,frequency and duration of spontaneous recurrent epilepsy , observed for 6 hours a day for 4 weeks;EEG was recorded on the 14th,28th and 36th day after modeling ,and the abnormal frequency of EEG in 1 h was counted . On the 6th day of modeling ,other 10 mice in each group were taken to detect the serum calcium level ,and the remaining 10 mice in each group were taken to detect the expressions of BDNF mRNA and protein in the hippocampus. RESULTS :Compared with normal group ,latency,frequency and duration of spontaneous recurrent epilepsy and the times of abnormal brain wave on the 14th,28th and 36th day after modeling were increased significantly in model group (P< 0.05). The serum calcium level , mRNA and proteinexpression of BDNF in hippocampus were increased E-mail:wangfang7699@126.com significantly (P<0.05). Compared with model group ,the latency,frequency,duration of spontaneous recurrent epilepsy and the times of abnormal brain wave on the 28th and 36th day after modeling were decreased significantly in single medication group(P<0.05),while serum calcium level ,mRNA and protein expression of BDNF in hippocampus were decreased significantly (P<0.05). Compared with single medication group ,the latency,frequency and duration of spontaneous recurrent epilepsy and the times of abnormal brain wave on the 28th and 36th day after modeling were increased significantly in agonist combination group (P<0.05),while serum calcium level ,mRNA and protein expressions of BDNF in hippocampus were increased significantly (P<0.05). CONCLUSIONS :Mulberry anthocyanin- 3- glucoside has a good protection effect on epilepsy model mice ,the mechanism of which may be associated with inhibiting the activation of hippocampal BDNF/TrkB pathway.
期刊: 2020年第31卷第03期
作者: 王芳,侯自立,韩冰,解国圣,张艳玲
AUTHORS: WANG Fang,HOU Zili,HAN Bing,XIE Guosheng ,ZHANG Yanling
关键字: 桑椹花青素-3-葡萄糖苷;癫痫;脑源性神经营养因子;酪氨酸激酶受体B;机制;小鼠
KEYWORDS: Mulberry anthocyanin- 3-glucoside;Epilepsy;Brain derived n eurotrophic factor ;Tyrosine kinase B ;Mechanism;
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