【摘要】 目的 利用非靶向代谢组学探究慢性高原缺氧致肺损伤的机制。方法 1.采用LC-MS/MS法分析研究探讨慢性高原缺氧致肺损伤组织的代谢变化；2.采用PCA和OPLS-DA法鉴定差异代谢物；3.通过KEGG富集分析法等方法鉴定标志物、分析代谢通路。结果 1.提取出2 489个峰，最终鉴定出2 454个峰；2.PCA图表明整个研究中存在低水平的仪器变化(即，良好的再现性)且通过OPLS-DA法检测到198种不同代谢物；3.这些潜在的生物标志物主要涉及嘌呤代谢、半胱氨酸和蛋氨酸代谢、丙酮酸代谢和氨基糖、核苷酸糖代谢等代谢途径。结论 1.代谢组学为鉴定肺损伤标志物提供了可能性；2.这198种代谢产物可能是肺损伤的潜在标志物；3.本实验采用非靶向代谢组学对慢性高原低氧所致的肺损伤的研究为寻找潜在的慢性高原低氧肺损伤代谢生物标志物提供了新的依据。更多还原

【Abstract】 Objective To explore the mechanism of chronic high altitude hypoxia-induced lung injury by non-targeted metabolomics.Methods 1.LC-MS/MS analysis was used to investigate the metabolic changes of lung tissue; 2.PCA and OPLS-DA methods were used to identify differential metabolites; 3.Marker identification and metabolic pathway analysis were performed by KEGG enrichment analysis.Results 1.2 489 peaks were extracted and 2 454 peaks were identified.2.PCA plot show that low levels of instrumental variation(i.e.,good reproducibility)are present across the study and 198 different metabolites were detected by OPLS-DA.3.KEGG analysis showed that these potential biomarkers mainly involved metabolic pathways such as purine metabolism, cysteine and methionine metabolism, pyruvate metabolism, amino sugar and nucleotide sugar metabolism.Conclusions 1.Metabolomics provides a possibility for the identification of lung injury markers; 2.These 198 metabolites might the potential markers of lung injury; 3.The study of untargeted metabolomics on lung injury caused by chronic altitude hypoxia in this study provides a new basis for the search for potential metabolic biomarkers of chronic altitude hypoxia lung injury.更多还原