Jiangxi University of Chinese Medicine Research Center for Differention and Development of Traditional Chinese Medicine (TCM) Basic Theory, Jiangxi Province Key Laboratory of TCM Etiopathogenisis, Nanchang 330004, China.
J Tradit Chin Med. 2023 Apr;43(2):274-285. doi: 10.19852/j.cnki.jtcm.20230201.001.
To investigate the mechanism of deficiency syndrome (YDS) by analyzing the liver metabolomic characteristics of three different deficiency rat models METHODS: Following the TCM etiology, for clinical features and pathological manifestations of modern medicine, three kinds of animal models of deficiency were induced and replicated. Totally 48 Sprague-Dawley (SD) male rats were randomly divided into blank group, irritation induced model group, Fuzi-Ganjiang induced model group, and thyroxine-reserpine induced model group. After successful development of model, the ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry was carried out to detect metabolites in each group. The metabolites of rat liver were analyzed for the characteristics of their biomarkers. The pathway enrichment analysis and metabolic network construction were performed through various online databases including Metabolite Biology Role, Human Metabolome Database, MetaboAnalyst, and Kyoto Encyclopedia of Genes and Genomes.
The SD rats in the experimental group showed symptoms like less weight gain, reduced diet and water intake, high body temperature, increased liver and kidney indexes, and abnormal liver and kidney tissue morphology. Moreover, the rats showed high increased levels of serum cyclic adenosine monophosphate, estradiol, alanine transaminase, and aspartate aminotransferase and decreased levels of cyclic guanosinc monophosphate and testosterone. We found four key interrelated metabolic pathways in the liver tissue metabolomics, including the biosynthesis of pantothenic acid and coenzyme A, and metabolism of alpha-linolenic acid metabolism, glycerophospholipid metabolism, and sphingolipid.
The liver and kidney YDS is closely related to the biosynthesis of pantothenic acid and CoA and abnormal metabolism of α-linolenic acid, glycerophospholipid, and sphingolipid in SD rats.
通过分析三种不同虚证大鼠模型的肝代谢组学特征，探讨虚证的发生机制。方法：根据中医病因病机，结合现代医学的临床特征和病理表现，诱导并复制三种动物模型。将 48 只雄性 SD 大鼠随机分为空白组、造模组、附子干姜诱导模型组、甲状腺素利血平诱导模型组。模型成功建立后，采用超高效液相色谱-四级杆飞行时间串联质谱法检测各组大鼠肝脏代谢物，分析大鼠肝脏代谢物的特征及其生物标志物。通过 Metabolite Biology Role、Human Metabolome Database、MetaboAnalyst、京都基因与基因组百科全书等多个在线数据库进行代谢通路富集分析和代谢网络构建。结果：实验组 SD 大鼠表现为体重增长缓慢、饮食和饮水量减少、体温升高、肝肾指数增加、肝肾组织形态异常等症状。同时，大鼠血清环磷酸腺苷、雌二醇、丙氨酸氨基转移酶和天门冬氨酸氨基转移酶水平升高，环磷酸鸟苷和睾酮水平降低。在肝组织代谢组学中发现了四个关键的相互关联的代谢途径，包括泛酸和辅酶 A 的生物合成以及α-亚麻酸代谢、甘油磷脂代谢、鞘脂代谢。结论：SD 大鼠的肝肾 YDS 与泛酸和辅酶 A 的生物合成以及α-亚麻酸、甘油磷脂、鞘脂代谢异常密切相关。
