UPLC-Q-TOF-MS profiling of the hippocampus reveals metabolite biomarkers for the impact of D1-3-n-butylphthalide on the lipopolysaccharide-induced rat model of depression
UPLC-Q-TOF-MS profiling of the hippocampus reveals metabolite biomarkers for the impact of D1-3-n-butylphthalide on the lipopolysaccharide-induced rat model of depression
复制标题
海马体的 UPLC-Q-TOF-MS 分析揭示了 D1-3-正丁基苯酞对脂多糖诱导的大鼠抑郁模型影响的代谢生物标志物
DOI：
10.2147/ndt.s203870
复制
发表时间：
2019-01-01
影响因子：
3.2
通讯作者：
Jiang, Pei
中科院分区：
文献类型：
--
作者：
Geng, Chunmei;Guo, Yujin;Jiang, Pei
目的：越来越多的证据表明炎症参与了抑郁症的病理机制。我们前期的基础研究证实了d1 -3-正丁基酞（NBP）具有抗炎作用。然而，在脂多糖（LPS）诱导的抑郁症大鼠模型中，研究海马组织中NBP参与的代谢物生物标志物的研究目前是有限的。因此，本研究的目的是确定海马代谢物生物标志物，以确定NBP在该抑郁症模型中的影响。材料与方法：将雄性Sprague-Dawley大鼠随机分为3组（n=6）：对照组、LPS诱导的大鼠抑郁模型（LPS）组和NBP参与的LPS诱导的大鼠抑郁模型（LPS+NBP）组。采用超高效液相色谱-质谱法测定海马代谢物。通过多变量统计分析确定三组海马代谢物的差异表达。结果：大多数鉴定的差异表达代谢物与氨基酸、脂质、能量和氧化应激代谢有关。此外，代谢物最终连接到不同的途径和代谢网络，这可能部分解释了抑郁症的病理生理过程。结论：本研究揭示了NBP的抗炎作用，并进一步阐明了炎症性抑郁的病理生理机制。
Purpose: An increasing body of evidence reveals that inflammation is involved in the pathological mechanisms of depression. Our previous basic research confirmed that D1-3-n-butylphthalide (NBP) possess anti-inflammatory properties. However, studies investigating metabolite biomarkers for the involvement of NBP in hippocampus tissue in the lipopolysaccharide (LPS)-induced rat model of depression are currently limited. Thus, the aim of this study was to identify metabolite biomarkers in the hippocampus for the impact of NBP in this model of depression.Material and methods: Male Sprague-Dawley rats were randomly allocated to one of the following three groups (n=6): Control, LPS-induced rat model of depression (LPS), and NBP involvement in the LPS-induced rat model of depression (LPS+NBP). Ultra-high-performance liquid chromatography-mass spectroscopy was used to determine the hippocampal metabolites. Multivariate statistical analysis was performed to identify differentially expressed hippocampal metabolites in the three groups.Results: Most of the identified differentially expressed metabolites were related to amino acid, lipid, energy, and oxidative stress metabolism. Additionally, metabolites were eventually connected to different pathways and metabolic networks, which may partly account for the pathophysiological process of depression.Conclusion: The present findings provide insight into the anti-inflammatory effects of NBP, and further elucidate the pathophysiological mechanisms underlying inflammation-induced depression.