摘要
目的:探讨β-细辛醚对抑郁模型大鼠行为学及丝裂原活化蛋白激酶磷酸酶-1(MKP-1),增强有丝分裂原和应激活化蛋白酶-1(MSK-1),cAMP反应元件结合蛋白(CREB)和B细胞淋巴瘤/白血病因子-2(Bcl-2)表达的影响。方法:60只2～3月龄SD大鼠随机分为正常对照组、模型组、氟西汀组和β-细辛醚组,每组15只。采用慢性轻度不可预见性应激加孤养复制抑郁模型,造模第2天开始,氟西汀组和β-细辛醚组灌胃给药,1次/d(氟西汀1.2 mg.kg-1.d-1,β-细辛醚25 mg.kg-1.d-1)。于实验第1,7,14,21天,分别进行体重、糖水消耗量检测和敞箱实验,对大鼠行为学改变进行评定。采用免疫组织化学染色检测MKP-1和Bcl-2蛋白表达,实时定量PCR对MKP-1,MSK-1,CREB和Bcl-2进行定量分析。结果:与模型组比较,氟西汀组和β-细辛醚组大鼠行为学指标显著改善,海马区MKP-1表达减弱、MSK-1,CREB和Bcl-2表达增强,差异有统计学意义(P<0.05)。结论:β-细辛醚可有效改善抑郁模型大鼠的抑郁症状,其机制可能与减少海马区MKP-1,增强MSK-1,CREB和Bcl-2蛋白表达有关。
Objective： To investigate the effects of beta-asarone on the behavior and the expressions of mitogen-activated protein kinase phosphatase-1 （MKP-1）, extracellular signal-regulated kinase （ERK） , mitogen and stress activated protein kinase-1 （MSK-1）, cAMP response element binding protein （CREB）, B cell Lymphomal/Leukemia-2 （Bcl-2） in the hippocampus of depression model rats. Method： Sixty adult Sprague- Dawley rats were randomly divided into 4 groups： the normal control group （NC）, the model control group （MC）, the/3-asarone group （A）, the fluoxetine control group （FC）, 15 in each one. Except those in the NC, the rest rats were singly housed and exposed on an unpredicted sequence of mild stressor. From the second day, A and FC group rats were administered with corresponding medicinal liquid everyday （ 1.2 mg ·kg^-1·d^-1 to the FC group, 25 mg·kg^-1·d^-1 to the A group） by gastro-gavage for 21 days. The rats＇body weight, sucrose consumption volume in the sucrose preference test, and times of grooming in the Open-field-test were detected on the 1, 7, 14, 21th day, respectively. The protein expressions of MKP-1 and Bcl-2 in the hippocampus were detected by immunohistochemical assay, while Real-time PCR for quantitative analysis of MKP-1, MSK-1, CREB and Bcl-2.Result： Compared with the MC group, the scores of A group and FC group in the open field test increased; the protein expressions of MKP-1 in the hippocampus decreased while MSK-1, CREB and Bcl-2 increased with statistical significance （P 〈 0. 05）. Conclusion ： Beta-asarone could obviously improve the depressive state of the model rats. Its mechanism might be correlated with decreasing the protein expressions of MKP-1, increasing MSK-1, CREB and Bcl-2 in the hippocampus.
出处
《中国实验方剂学杂志》
CAS
北大核心
2013年第16期272-277,共6页
Chinese Journal of Experimental Traditional Medical Formulae
基金
黑龙江省教育厅科学技术研究面上项目(12521638)
关键词
Β-细辛醚
抑郁
丝裂原活化蛋白激酶磷酸酶-1
有丝分裂原和应激活化蛋白激酶-1
cAMP反应元件结合
蛋白
B细胞淋巴瘤
白血病因子-2
beta-asarone
depression
mitogen-activated protein kinaseextracellular signal-regulated kinase （ERK）
mitogen and stress activated proteinresponse element binding protein （CREB）
B cell Lymphomal/Leukemia-2 （Bcl-2）phosphatase-1 （ MKP-1 ）
kinase-1 （MSK-1）
cAMP
