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通过代谢组学评价痛泻要方对肠易激综合征(irritable bowel syndrome,IBS)大鼠模型血清内源性物质代谢干预效应,寻找潜在的生物标志物并分析其代谢途径,探讨痛泻要方的作用机制及病证模型的证候本质。将40只Wistar大鼠复制为IBS模型,随机分为模型对照组和痛泻要方给药组4组,另设空白对照组10只。痛泻要方(低、中、高)组分别灌胃剂量为0.203,0.406,0.812 g·m L~(-1)的痛泻要方,空白对照组及模型对照组给予等体积的生理盐水,每日1次,连续2周。各组大鼠于灌胃第0,15天采集血清,经处理后供UPLC-Q-TOF-MS进行代谢组学分析。鉴定出8个潜在生物标志物,分析出8条主要代谢通路,其与IBS疾病的神经递质代谢、炎性免疫、脑神经功能及能量代谢等有关,痛泻要方对IBS疾病的作用机制可能涉及血清素突触和色氨酸代谢、半胱氨酸和甲硫氨酸代谢、甘油磷脂代谢、烟酸和烟酰胺代谢等过程,其可能是IBS模型肝旺脾虚证的生物学基础。
Metabolomics was used to evaluate the effect of Tongxie Yaofang on serum endogenous substance metabolism in the rat model of irritable bowel syndrome (IBS) by searching for potential biomarkers and analyzing the metabolic pathways, The mechanism of action and the nature of syndromes of disease and syndrome model. Forty Wistar rats were duplicated into IBS model and randomly divided into four groups: model control group and TongxieYaoFang administration group, and another 10 blank control group. Tongxuyaofang (low, middle and high) group were given intragastric dose of 0.203, 0.406 and 0.812 g · m L ~ (-1) respectively. The control group and the model control group were given equal volume of normal saline , 1 day, for 2 weeks. Serum was collected on the 0th and 15th day after intragastric administration, and the metabolites were analyzed by UPLC-Q-TOF-MS. Eight potential biomarkers were identified, and eight major metabolic pathways were identified. They were related to neurotransmitter metabolism, inflammatory immunity, brain nerve function and energy metabolism in IBS, and the mechanism of action of TongxieYaoFang on IBS disease It may be involved in serotonin synapse and tryptophan metabolism, cysteine and methionine metabolism, glycerophospholipid metabolism, nicotinic acid and nicotinamide metabolism process, which may be the biological basis of IBS model liver wang spleen deficiency syndrome.