摘要
目的:观察异常黑胆质成熟剂(ASMq)对抑郁症模型大鼠海马ERK信号通路的影响,探讨异常黑胆质成熟剂抗抑郁作用机制。方法:84只雄性SD大鼠,随机分为6组:正常对照组、抑郁症模型组、阳性对照组(氟西汀,3.5mg/kg)及异常黑胆质成熟剂低、中、高剂量组(浓度分别为1.5、3.0、6.0g/kg),每组14只。除正常对照组外,其它组采用慢性不可预见性温和应激(CUMS)诱导建立大鼠抑郁症模型,阳性对照组和异常黑胆质成熟剂各剂量组连续灌胃给药24天,1次/天。通过Open-field实验和糖水消耗实验来评估大鼠抑郁活动状态。末次给药24h后断头处死大鼠、迅速分离海马组织、冻存备用,蛋白印迹法(Western blot)检测大鼠海马p-ERK1/2,ERK1/2表达。结果:应激结束后与正常对照组相比,抑郁症模型组大鼠体重增加量降低、糖水消耗量减少,水平穿越格数、竖立次数均明显降低,处于抑郁状态;各组之间ERK1/2的表达没有显著性差异。与正常对照组相比,抑郁症模型组大鼠海马p-ERK1/2表达明显下降,差异有显著性。与抑郁症模型组相比,阳性对照组和异常黑胆质成熟剂中、高剂(浓度为3.0、6.0g/kg)量组大鼠体重增加量上升、糖水消耗量升高,水平穿越格数、竖立次数均明显增加;与抑郁症模型组相比,阳性对照组、异常黑胆质成熟剂中剂(浓度为3.0 g/kg)量组海马组织p-ERK1/2表达量明显升高,差异有显著性。结论:异常黑胆质成熟剂可能是通过调节ERK信号通路来发挥抗抑郁作用。
Objective： To observe The effect of Abnormal Savda Munziq （ASMq） on ERK signal pathway in the hippocampus of depression Rat models. Methods： The 84 SD rats were randomly divided into 6 groups with 14 in each group：normal control group , depression animal model group , high, moderate and low ASMq granules dose groups （6.0,3.0,1. 5 g/kg） and the positive control group （ Fluoxetine,3.5 rag/ kg）. Except the normal control group, the rats in all other groups were given chronic unpredictable mild stress （CUMS） to build the depres sion animal models. The positive control group and the ASMq groups were orally administrated once a day for 24 days. The behavioral status of rats was evluated by Open-field test and sugar consumption experiment. 24h after the last administration, all the rats were executed, the hippecampal tissue separated and cryopreserved for standby. The protein expression of p-ERK1/2, ERK1/2 in the hippocampus of rats were tested by Western-blot. Results： After CUMS, the body weight gain , sugar consumption , horizontal crossing numbers and erection times of depression group were significantly decreased than normal control group（ P 〈 0.01 ）, so the depression model group was in an obvious depressive state. The level of ERK1/2 in each group were unchanged. The content of p- ERK1/2 protein expression levels in hippocampus of depression group were significantly lower than normal greup（P 〈0.01, P 〈0.05）. The body weight gain , sugar consumption , horizontal crossing numbers and erection times of positive control group, groups of ASMq granules for high（6.0g/kg）, medium（3.0g/kg） were significandy increased than depression group （P 〈 0.01 ）. The content of p- ERK1/2 in positive control group, moderate （3.0g/kg） were significandy higher than depression group （P 〈 0.01, P 〈 0.05 ）. Conclusion： The anti-depression effect of Abnormal Savda Manziq （ASMq） may be related to regulating the cAMP-PKA signal pathway.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2014年第1期112-116,共5页
Pharmacology and Clinics of Chinese Materia Medica
基金
国家自然科学基金项目(81360667)
关键词
异常黑胆质成熟剂
抑郁症
ERK信号通路
abnormal Savda Muuziq（ASMq,异常黑胆质成熟剂）
depression animal model
ERKsignal pathway
