灵芝多糖对辐射损伤小鼠影响的胸腺代谢组学分析

Thymic Metabolomics for Effect of Ganoderma Polysaccharides on Radiation-injured Mice

目的:运用代谢组学方法分析灵芝多糖对辐射损伤小鼠内源性物质代谢的影响,寻找潜在的生物标志物并分析其代谢途径,探讨其作用机制。方法:将30只小鼠随机分为正常组、模型组和灵芝多糖组(给药剂量96 mg·kg^-1),每组10只,前两组给予生理盐水,连续灌胃14 d,在第7天灌胃后2 h,除正常组外,模型组和灵芝多糖组小鼠以X射线进行全身照射。利用UPLC-Q-TOF-MS检测胸腺组织中内源性小分子代谢物,利用主成分分析(PCA)和正交偏最小二乘法-判别分析(OPLSDA)比较正常组、模型组以及灵芝多糖组内源性小分子代谢物的变化情况,对差异代谢物进行京都基因与基因组百科全书(KEGG)代谢通路分析。结果:鉴定出34个潜在生物标志物,与模型组相比,发现灵芝多糖组对L-谷氨酸、牛磺酸、磷脂酰胆碱(PC)和溶血磷脂酰胆碱(Lyso PC)等均具有显著的逆转趋势,分别参与牛磺酸和亚牛磺酸代谢、甘油磷脂代谢以及D-谷氨酰胺和D-谷氨酸代谢。结论:灵芝多糖可能通过改善辐射模型小鼠胸腺中相关潜在生物标志物表达及其相关代谢通路来发挥辐射防护作用。

Objective:To observe the effect of Ganoderma polysaccharides(GP)on endogenous substance metabolism in radiation-injured mice by metabolomics,so as to find potential biomarkers and analyze their metabolic pathways,and to explore its mechanism of action.Method:Thirty mice were randomly divided into normal group(normal saline),model group(normal saline)and GP group(dose of 96 mg·kg^-1)for 14 days of continuous intragastric administration,10 mice in each group,2 h after the intragastric administration on the 7 thday,mice in the model group and GP group were subjected to whole body irradiation by X-rays,except the normal group.UPLC-Q-TOF-MS was used to detect endogenous small molecule metabolites in thymus tissue of mice.Principal component analysis(PCA)and orthogonal partial least squares discriminant analysis(OPLS-DA)were used to compare the changes of endogenous small molecule metabolites in thees three groups,these differential metabolites among the three groups were analyzed by Kyoto encyclopedia of genes and genomes(KEGG)metabolic pathway method.Result:A total of 34 potential biomarkers were identified,compared with the model group,it was found that the GP group had a significant reversal trend on L-glutamic acid,taurine,phosphatidylcholine(PC)and lysophosphatidylcholine(LysoPC),etc.They were involved in taurine and hypotaurine metabolism,D-glutamine and D-glutamate metabolism,glycerophospholipid metabolism.Conclusion:GP can play a role in radiation protection by improving the expression of related potential biomarkers and related metabolic pathways in thymus of radiation-injured mice.