柴胡皂苷A对脑损伤大鼠认知功能的干预及机理研究  

Intervention and mechanism study of saikosaponin A on cognitive function in brain injury rats

作　　者：侯蕊[1] 曹俊杰[1] 王义围[1] 赵翠[1] 张孔雁 蒋海森[1] 冯玉梅[1] 李久民 卢竞前 HOU Rui;CAO Jun-jie;WANG Yi-wei;ZHAO Cui;ZHANG Kong-yan;JIANG Hai-sen;FENG Yu-mei;LI Jiu-rain;LU Jing-qian(Department of Geriatrics,Affiliated Hospital of Chengde Medical College Chengde 067000,Hebei Province,China;Department of Cardiology,The First People＇s Hospital of Kunming,Kunming 650000,China;Department of Internal Medicine,Chengde County Hospital,Chengde 067400,Hebei Province,China)

机构地区：[1]承德医学院附属医院老年病科,河北承德067000 [2]昆明市第一人民医院心内科,昆明650000 [3]承德县医院内科,河北承德067400

出　　处：《中国临床药理学杂志》2018年第22期2628-2630,共3页The Chinese Journal of Clinical Pharmacology

摘　　要：目的探讨柴胡皂苷A对脑损伤大鼠认知功能的干预及机制。方法 30只SD大鼠经颅脑撞击建立中度皮层损伤模型后随机分为模型组和实验组,各15只,分别灌胃柴胡皂苷A 5 mg·kg^(-1)和等量生理盐水;另外10只为假手术组不进行颅脑撞击,灌胃等量生理盐水,各组均连续干预14 d。评估大鼠脑损伤后的神经功能,Morris水迷宫系统测定大鼠认知功能,酶联免疫吸附实验(ELISA)检测大鼠海马组织白介素-1β(IL-1β)及脑源性神经生长因子(BDNF)含量,蛋白免疫印迹法检测大鼠海马组织Janus激酶(JAK)/信号转导转录激活因子3(STAT3)通路蛋白表达。结果实验组脑损伤后神经功能评分均高于模型组,且随脑损伤后时间的延长神经功能评分呈逐渐升高趋势(P <0. 05)。假手术组、模型组及实验组穿台次数为(14. 05±3. 46),(7. 43±2. 87),(10. 41±3. 32)次,与模型组比较,实验组大鼠逃避潜伏期缩短,穿台次数增多(P <0. 05)。假手术组、模型组和实验组的BDNF含量为(712. 51±12. 63),(326. 45±10. 54),(621. 48±16. 52) pg·mg^(-1); IL-1β分别为(1. 56±0. 23),(3. 84±0. 25),(1. 93±0. 26) pg·mg^(-1),差异均有统计学意义(均P <0. 05)。假手术组、模型组及实验组海马组织JAK蛋白相对表达量为0. 71±0. 12,1. 87±0. 35,0. 96±0. 22,STAT3蛋白相对表达量为0. 36±0. 04,0. 98±0. 12,0. 51±0. 04。模型组海马组织JAK、STAT3蛋白含量高于假手术组,而实验组海马组织JAK、STAT3蛋白低于模型组(P <0. 05)。结论柴胡皂苷A可有效改善脑损伤大鼠的认知功能和神经功能,可能与其抑制海马组织JAK/STAT3通路活化有关。Objective To study the intervention and mechanism of sai- kosaponin A on cognitive function in brain injury rats. Methods Thirty rats underwent craniocerebral injury to establish a model of moderate cortical injury and were divided into model group and test group randomly, 15 cases in each group, which were gavaged saikosaponin A 5 mg· kg^-1 and the same amount of normal saline respectively; the other 10 cases of rats were sham operation group, which had not craniocerebral injury and gavaged with the equivalent normal saline, all groups had continuous in- tervention for 14 d. Neurological function of rats was assessed after brain injury; Morris water maze system was used to measure the cognitive function of rats; enzyme- linked immunosorbent assay （ELISA） was used to detect the levels of interleukin - 1β（ IL - 1β） and brain - derived nerve growth factor （BDNF） in rat hippocampus ; Western blot （WB） was used to detect the expression of Janus kinase/signal transducer and activator of transcription 3 （JAK/STA33） pathway proteins in rat hippocampus. Results The neurological function score in test group was higher than those in model group after brain injury, and neurological function scores increased gradually with the prolongation of the time after brain injury （P 〈 O. 05 ）. The passing platform times of sham operation group, model group and test group were 14. 05 ± 3.46, 7.43 ± 2. 87 10. 41 ± 3. 32, compared with model group, the escape incubation of test group shortened, the passing platform times increased （P 〈 0. 05 ）. The content of BDNF in hippocampus of sham operation group, model group and test group were （712. 51 ± 12. 63）, （326. 45 ± 10. 54）, （621.48 ± 16. 52） pg·mg^-1, the content of IL - 1β were （ 1.56 ± 0. 23 ）, （3.84 ± 0. 25 ）, （ 1.93 ± 0. 26 ） pg·mg^-1, the difference was statistically significant （P 〈 0. 05 ）. The janus kinase （JAK） proteins expression in hippocampus of sham operation group, model group and test group we

关 键 词：脑损伤 柴胡皂苷A 认知 神经功能 Janus激酶/信号转导与转录激活因子3通路 

分 类 号：R28[医药卫生—中药学]