基于代谢组学分析溃疡性结肠炎模型大鼠结肠组织代谢特征及疾病机制  被引量:1

The metabolic characteristics and disease mechanism of colon tissue in ulcerative colitis model rats based on metabolomic

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作  者:王佳林 马秀兰 韩金荣[3] 朱西杰[3] WANG Jia-Lin;MA Xiu-Lan;HAN Jin-Rong(School of Nursing,Ningxia Medical University,Yinchuan 750004,Ningxia,China)

机构地区:[1]宁夏医科大学护理学院,宁夏银川750004 [2]宁夏医科大学中医药现代化教育部重点实验室,宁夏银川750004 [3]宁夏医科大学中医学院,宁夏银川750004

出  处:《中国老年学杂志》2024年第2期372-376,共5页Chinese Journal of Gerontology

基  金:2017年国家自然科学基金项目(No.81760863);2019年国家自然科学基金项目(No.81960859);2017年宁夏回族自治区高等学校教育厅建设项目(No.NGY2017111)。

摘  要:目的研究溃疡性结肠炎(UC)模型大鼠结肠组织代谢物质差异,探索UC疾病机制。方法采用2,4,6-三硝基苯磺酸(TNBS)-乙醇复合造模法建立UC大鼠模型,采用超高效液相色谱-四极杆-飞行时间串联质谱法(UPLC-Q-TOF-MS/MS)技术检测,结合多元统计分析方法,进行代谢组学数据分析。结果根据筛选条件变量权重(VIP)>1、P<0.05筛选差异性代谢物,筛选结果中上调物质18种:苯乙酰甘氨酸、N-(邻甲苯酰)甘氨酸、对甲苯基硫酸、溶血磷脂酰乙醇胺(LPE,18∶1/0∶0)、2-[(5Z,8Z,11Z,14Z,17Z)-icosa-5,8,11,14,17-戊烯氧基]丁酸、溶血磷脂酰胆碱(LPC,18∶2/0∶0)、孕烯醇、LPC(0∶0/18∶1)、LPE(0∶0/18∶2)、Thr-Glu-Leu-Lys、LPC(16∶1/0∶0)、1-(13Z,16Z-docosadienoyl)-glycero-3-phosphate、Hecogenin、LPE(0∶0/16∶1)、LPE(18∶2/0∶0)、LPE(14∶0/0∶0)、10-脱氧甲霉素、Glycerophospho-N-Palmitoyl Ethanolamine;下调物质2种:[(2S)-2-hexadecanoyloxy-3-tetradecanoyloxypropyl](6Z,9Z,12Z,15Z)-octadeca-6,9,12,15-tetraenoate、LPC(O-16∶1/0∶0)。主要涉及氨基酸代谢、脂质代谢两个代谢途径。结论UC疾病发生过程中与氨基酸、脂质物质代谢异常有关,其疾病机制可能与苯丙氨酸代谢途径发生改变及脂质中甘油磷脂类、三酰甘油代谢异常相关联。Objective To study the differences of metabolites in colon tissue of ulcerative colitis(UC)model rats,and to explore the disease mechanism of UC.Methods The UC rat model was established by 2,4,6-trinitrobenzenesulfonic acid(TNBS)-ethanol composite modeling method.The metabolomics data were analyzed by ultra performance Liquid chromatography(UPLC)-quadrupole(Q)-time-of-flight(TOF)-mass spectrometry(MS),combined with multivariate statistical analysis methods.Results Differential metabolites were screened according to the screening condition variable weight(VIP)>1,P<0.05.There were 18 up-regulated substances in the screening results:phenylacetylglycine,N-(o-toluoyl)glycine,p-tolyl sulfate,lysophosphatidyl ethanolanine(LPE,18∶1/0∶0),2-[(5Z,8Z,11Z,14Z,17Z)-icosa-5,8,11,14,17-pentaenyloxy]butanoic,lysophosphatidylcholine(LPC,18:2/0:0),pregnenols,LPC(0:0/18:1),LPE(0:0/18:2),Thr-Glu-Leu-Lys,LPC(16:1/0:0),1-(13Z,16Z-docosadienoyl)-glycero-3-phosphate,Hecogenin,LPE(0:0/16:1),LPE(18:2/0:0),LPE(14:0/0:0),10-deoxymethycin,Glycerophospho-N-Palmitoyl Ethanolamine.Two down-regulated substances:[(2S)-2-hexadecanoyloxy-3-tetradecanoyloxypropyl](6Z,9Z,12Z,15Z)-octadeca-6,9,12,15-tetraenoate,LPC(O-16:1/0:0).It mainly involved two metabolic pathways:amino acid metabolism and lipid metabolism.Conclusions UC is associated with abnormal amino acid and lipid metabolism in the course of disease,and its disease mechanism might be related to changes in phenylalanine metabolic pathway and abnormal metabolism of glycerophospholipids and triglycerides in lipids.

关 键 词:溃疡性结肠炎 超高效液相色谱-四极杆-飞行时间串联质谱法(UPLC-Q-TOF-MS/MS) 代谢组学 氨基酸代谢 脂质代谢 

分 类 号:R285.5[医药卫生—中药学]

 

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