【摘要】 旨在解析热应激下猪睾丸间质细胞代谢物的变化情况。设置对照组(NC,37℃)和热应激组(HS,43℃80 min)，收集猪睾丸间质细胞，采用超高效液相色谱技术鉴定各组代谢物，以变量投影重要度(VIP)>1.0，差异倍数(FC)>1.5或FC<0.667且P<0.05为标准鉴定差异代谢物，并进行KEGG功能富集分析。结果:针对HS组与NC组鉴定差异代谢物，正离子(POS)和负离子(NEG)模式下共鉴定出539个差异代谢物，表明热应激后猪睾丸间质细胞代谢发生显著变化;对鉴定到的差异代谢物进行KEGG富集分析表明，POS模式下主要富集的通路包括花生四烯酸代谢、谷胱甘肽代谢、半胱氨酸和蛋氨酸代谢等，其中代谢物整体呈下调趋势; NEG模式下则显著富集于甘油磷脂代谢、铁死亡、不饱和脂肪酸生物合成、炎症介质对TRP通道的调控及胆汁分泌等通路，代谢物呈上调趋势，两组差异代谢物在POS与NEG模式下涉及的通路及表达变化趋势存在显著差异，提示其代谢调控机制具有模式特异性。综上，热应激改变了猪睾丸间质细胞代谢通路的组学特征，主要表现为干扰脂质代谢和激活铁死亡代谢途径，研究结果为进一步探究热应激损伤猪睾丸间质细胞结构和功能的分子机理奠定理论基础。更多还原

【Abstract】 This study aimed to analyze the alterations in metabolites of porcine Leydig cells under heat stress. A control group(NC,37 ℃)and a heat stress group(HS,43 ℃ for 80 min) were established. Metabolites from porcine Leydig cells were collected and identified using ultraperformance liquid chromatography. Then,differential metabolites were screened based on the criteria of VIP > 1. 0,FC> 1. 5 or FC<0. 667,and P<0. 05,followed by KEGG functional enrichment analysis. The results were as follows: A total of 539 differential metabolites were identified between the HS and NC groups in both positive(POS) and negative(NEG) ion modes,indicating significant metabolic changes in Leydig cells after heat stress. The KEGG enrichment analysis revealed that,in the POS mode,pathways such as arachidonic acid metabolism,glutathione metabolism,and cysteine and methionine metabolism were prominently enriched,with most metabolites showing a downregulated trend. In the NEG mode,pathways including glycerophospholipid metabolism,ferroptosis,biosynthesis of unsaturated fatty acids,inflammatory mediator regulation of TRP channels,and bile secretion were significantly enriched; and the associated metabolites were predominantly upregulated. The pathways and expression trends of differential metabolites differed markedly between the two ionization modes,suggesting modespecific metabolic regulatory mechanisms. The results indicated that heat stress altered the metabolomic profile of porcine Leydig cells,mainly manifested as disturbed lipid metabolism and activation of ferroptosisrelated pathways. These findings laid a theoretical foundation for further elucidating the molecular mechanisms by which heat stress impairs the structure and function of porcine Leydig cells.更多还原