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目的探讨异常黑胆质成熟剂对抑郁症模型大鼠大脑细胞外信号调控激酶信号转导通路(ERK)的影响。方法选取Sprague-Dawley雄性大鼠84只,随机分为6组:正常对照组、阳性对照组、抑郁症模型组及异常黑胆质成熟剂低、中、高剂量组(ASMq低、中、高分别为1.5、3.0、6.0g·kg-1·d-1,连续给药4w),每组14只。除正常对照组外,其余各组均采用轻度不可预见性慢性应激刺激(Chronic mild unp redictable stress,CMUS)建立抑郁症大鼠模型,通过体质量测量、糖水摄取量综合评价大鼠行为学改变,在对ERK信号转导通路中Ras和RSK蛋白表达水平测量的基础上,采用重复测量和单因素方差分析方法,揭示异常黑胆质成熟剂的抗抑郁作用。结果与正常对照组比较,抑郁症模型组体质量增幅明显降低(P<0.05),糖水摄入量显著降低(P<0.05),差异均有统计学意义。与正常对照组比较,抑郁症模型组大鼠海马Ras和RSK蛋白表达显著降低(P<0.05),与抑郁症模型组比较,异常黑胆质成熟剂低、中、高剂量组与阳性对照组海马Ras和RSK蛋白表达显著升高(P<0.05),差异均有统计学意义。结论异常黑胆质成熟剂可能通过上调Ras/RSK/ERK信号转导通路起到抗抑郁作用。
Objective To investigate the effect of abnormal savda-mature agent on extracellular signal-regulated kinase signal transduction pathway (ERK) in the rat model of depression. Methods 84 Sprague-Dawley male rats were randomly divided into 6 groups: normal control group, positive control group, depression model group and abnormal savda mature agent low, medium and high dose groups (ASMq low, medium and high Respectively 1.5,3.0,6.0g · kg-1 · d-1, continuous administration 4w), 14 in each group. In addition to the normal control group, the rest of the groups were used to establish a model of depression rats with mild unpredictable chronic unpredictable stress (CMUS). Through the body weight measurement, Based on the measurement of Ras and RSK protein expression levels in ERK signal transduction pathway, repeated measures and one-way ANOVA were used to reveal the antidepressant effect of abnormal savda mature agent. Results Compared with the normal control group, the increase of body mass in depression model group was significantly lower (P <0.05) and the intake of syrup was significantly lower (P <0.05), the differences were statistically significant. Compared with the normal control group, the expressions of Ras and RSK in hippocampus of depression model group were significantly decreased (P <0.05). Compared with the depression model group, the low, medium and high dose of abnormal savda maturation agent group and the positive control group The protein expressions of Ras and RSK in hippocampus were significantly increased (P <0.05), the differences were statistically significant. Conclusion Abnormal savda may play an antidepressant effect by up-regulating Ras / RSK / ERK signal transduction pathway.