摘要
目的探讨丁苯酞对大鼠神经细胞凋亡的保护作用及其机制研究。方法选用90只SD大鼠,随机分为给药组、对照组和健康组,每组30只。对给药组和对照组大鼠使用10%水合氯醛麻醉(剂量为0.5mL/100g),麻醉完成后,对大鼠双侧海马区位置进行准确定位后,将浓度为5μL(1μg/μL)Aβ1-42注入造模。将配置的丁苯酞与食用麻油混合配制成悬浊液。造模完成后,分别给予不同的处理方法,给药组按75mg/kg比例对大鼠进行灌胃给药,1次/d。对照组按同等比例灌胃给予生理盐水,1次/d。健康组为正常健康组,不给予任何手术和药物处理。取大鼠脑组织分为两部分,一部分经固定、脱水、石蜡包埋后制得厚度约5μm切片。采用TUNEL染色法对脑组织细胞凋亡进行检测;并使用H&E染色法观察各组大鼠脑组织细胞;采用Western Blot法检测各组脑组织MAPK、Erk和P38的蛋白表达水平,并使用RT-PCR法检测MAPK、Erk和P38的mRNA表达水平。结果30d后,给药组大鼠脑组织细胞凋亡明显少于对照组及健康组。给药组大鼠MAPK、Erk和P38的蛋白表达水平明显低于对照组但高于正常健康组(P<0.05)。使用RT-PCR法检测MAPK、Erk和P38的mRNA表达水平发现,给药组大鼠MAPK、Erk和P38的mRNA水平明显低于对照组但高于正常健康组(P<0.05)。对照组大鼠达到学会标准次数与健康组比较明显升高(P<0.05)。与对照组比较,给药组大鼠达到学会标准次数明显降低(P<0.05)。结论丁苯酞对Aβ1-42处理的大鼠脑组织细胞凋亡具有保护作用,通过抑制大鼠脑组织MAPK,Erk和P38的表达发挥作用。
Objective To investigate the protective effect and mechanism of butylphthalide on nerve cell apoptosis in rats.Methods 90 SD rats were randomly divided into the medication administration group,control group and the healthy group in which 30 rats in each group.The medicine group and control group were anesthetized with 10%chloral hydrate（at a dose of 0.5mL/100g）.After successful anesthesia,bilateral hippocampal area of in rats were accurate positioned,a 5μL（1μg/μL）concentration of Aβ1-42 was injected for molding.The configuration of butylphthalide and oil was mixed into suspension.After the model was completed,the rats were given different treatment,and the drug group was administered with 75mg/kg for 1time per day.The control group was given normal saline by the same ratio for 1times a day.The healthy group was deal with the normal meal,without any operation and drug treatment.The brain tissue of rats was divided into two parts,one part was fixed,dehydrated,and embedded in paraffin,and the thickness of 5μm was obtained.TUNEL staining was used to detect the apoptosis of brain tissue;and HE staining was used to observe the rat brain tissue cells;Western blot was used to detect the MAPK,ERK and P38 protein expression level and RT-PCR was detected the expression level of MAPK and ERK and P38 mRNA expression levels.Results After 30 d,the apoptosis of the brain tissue of rats in the administration group was significantly less than that in the control group and the blank group.The protein expression levels of MAPK,Erk and P38 were significantly lower in the control group than in the control group but higher than those in the control group（P〈0.05）.The P38 expression levels of MAPK,Erk and mRNA were detected by RT-PCR,and the levels of MAPK,Erk and mRNA of P38 in rats were significantly lower than those in the control group but higher than those in the normal healthy group（P〈0.05）.In control group,the number of standards and health group was significantly higher（P〈0.05）.Compared with the con
作者
齐凡星
胡莹
卢军栋
康丽娟
李志安
张会朵
Qi Fanxin Hu Ying Lu Jundong Kang Lijuan Li Zhian Zhang Huiduo(The Second Depart- ment of Neurology, the First Center Hospital of Baoding City, Baoding 071000, China The Third Depart- ment of Cardiology, the First Center Hospital of Baoding City, Baoding 071000, China)
出处
《贵州医药》
CAS
2016年第11期1132-1134,共3页
Guizhou Medical Journal
关键词
阿兹海默
凋亡
丁苯酞
MAPK
Alzheimer＇s disease
Apoptosis
Dl-3n-butylphthalide
MAPK
