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目的建立脾气虚证大鼠模型,分析脾气虚证的代谢通路,探究内源性代谢产物变化与脾气虚证的关系。方法采用苦寒泻下、劳倦过度和饥饱失常复合因素方法建立并评价脾气虚证大鼠模型,检测其血清中肌酸磷酸激酶活性;对大鼠尿液进行~1H-NMR检测,以变化倍数(fold change,FC)>1.2,结合独立样本t检验(P<0.05)的统计学方法筛选脾气虚证模型组和对照组的差异代谢物,进行代谢通路分析与富集分析。结果脾气虚证模型建立成功;模型组的肌酸磷酸激酶活性低于对照组(P<0.05);从主成分分析(PCA)结果得出模型组和对照组的代谢产物得到明显区分;筛选出33种差异代谢物,主要参与的代谢通路涉及能量代谢、氨基酸代谢、核苷酸代谢,同时对肠道菌群存在干扰。结论脾气虚主要扰乱了大鼠的能量代谢通路(三羧酸循环、糖酵解、脂质氧化),抑制了供能作用,导致大鼠出现疲乏和体质量增长抑制的症状。
Objective To establish a rat model of spleen deficiency syndrome and to analyze the metabolic pathway of spleen deficiency syndrome and to explore the relationship between changes of endogenous metabolites and spleen deficiency syndrome. Methods The rat model of spleen-qi deficiency syndrome was established and evaluated by compounding factors of bitter cold and diarrhea, overwork and starvation, and the creatine phosphokinase activity in serum was detected. The urine of rats was detected by ~ 1H-NMR and the changes of fold (fold change, FC)> 1.2. The differential metabolites of the model group and the control group were screened by statistical methods of independent sample t test (P <0.05), and the metabolic pathway analysis and enrichment analysis were performed. Results The model of spleen deficiency syndrome was successfully established. The activity of creatine phosphokinase in model group was lower than that in control group (P <0.05). The results of principal component analysis (PCA) showed that the metabolites of model group and control group were obviously distinguished. 33 kinds of differential metabolites, the main metabolic pathways involved in energy metabolism, amino acid metabolism, nucleotide metabolism, while interfering with the intestinal flora. Conclusion Spleen deficiency mainly disrupts the energy metabolism pathway (tricarboxylic acid cycle, glycolysis, lipid oxidation) in rats, suppresses the energy supply and leads to the symptoms of tiredness and inhibition of growth of body weight in rats.