基于代谢组学技术，槲皮素在慢性不可预测的轻度应激大鼠模型中调节肝脏代谢特征,Food & Function

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基于代谢组学技术，槲皮素在慢性不可预测的轻度应激大鼠模型中调节肝脏代谢特征
Food & Function ( IF 5.1 ) Pub Date : 2023-01-18 , DOI: 10.1039/d2fo03277e
Siqi Jia ₁ , Ruijuan Wang ₁ , Dongyan Zhang ₁ , Zhiyu Guan ₁ , Tingting Ding ₁ , Jingnan Zhang ₁ , Xiujuan Zhao ₁

Affiliation

抑郁症是最普遍的精神疾病，其发病机制目前尚不清楚。目前，对抑郁症发病机制的研究主要集中在大脑。肝脏可以通过以下方式调节大脑功能肝脑轴，表明肝脏在抑郁症的发展中起着重要作用。本研究旨在基于非靶向代谢组学技术探讨槲皮素对慢性不可预知轻度应激（CUMS）诱导的大鼠肝脏代谢变化的保护作用及其机制。在这项研究中，96 只雄性大鼠被分为六组：对照组、不同剂量的槲皮素（10 毫克/千克体重或 50 毫克/千克体重）、CUMS 和 CUMS + 不同剂量的槲皮素。在 CUMS 建模 8 周后，收集肝脏样本用于代谢组学分析。共鉴定出 17 种改变的代谢物，包括D-谷氨酸、S-腺苷甲硫氨酸、石胆酰甘氨酸、L-同型半胱氨酸、前列腺素 PGE2、白三烯 E4、胆酸、5-甲基四氢叶酸、牛磺鹅脱氧胆酸、S-腺苷同型半胱氨酸、脱氧胆酸、叶酸、L-蛋氨酸、白三烯 C5、雌三醇-17-葡萄糖醛酸、PE 和 PC，表明蛋氨酸代谢、胆汁酸代谢和磷脂酰胆碱生物合成是参与 CUMS 诱导的肝脏代谢紊乱的主要途径。肝脏甲基化损伤可能在抑郁症的病理生理学中发挥作用，首次发现肝脏甲硫氨酸代谢异常就证明了这一点。肝胆汁酸的异常变化可能为涉及微生物群-肠-脑轴的抑郁症发病机制提供更有力的证据，表明肝脏参与抑郁症的发展并可能成为治疗目标。槲皮素治疗减轻了 CUMS 引起的肝脏代谢紊乱，表明槲皮素可能通过调节肝脏代谢来预防抑郁症。

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Quercetin modulates the liver metabolic profile in a chronic unpredictable mild stress rat model based on metabolomics technology

Depression is the most prevalent psychiatric disease, and its pathogenesis is still unclear. Currently, studies on the pathogenesis of depression are mainly focused on the brain. The liver can modulate brain function via the liver–brain axis, indicating that the liver plays an important role in the development of depression. This study aims to explore the protective effect of quercetin against chronic unpredictable mild stress (CUMS)-induced metabolic changes and the corresponding mechanisms in the rat liver based on untargeted metabolomics technology. In this study, 96 male rats were divided into six groups: control, different doses of quercetin (10 mg per kg bw or 50 mg per kg bw), CUMS, and CUMS + different doses of quercetin. After 8 weeks of CUMS modeling, the liver samples were collected for metabolomics analysis. A total of 17 altered metabolites were identified, including D-glutamic acid, S-adenosylmethionine, lithocholylglycine, L-homocystine, prostaglandin PGE2, leukotriene E4, cholic acid, 5-methyltetrahydrofolic acid, taurochenodeoxycholic acid, S-adenosylhomocysteine, deoxycholic acid, folic acid, L-methionine, leukotriene C5, estriol-17-glucuronide, PE, and PC, indicating that methionine metabolism, bile acid metabolism, and phosphatidylcholine biosynthesis are the major pathways involved in CUMS-induced hepatic metabolic disorders. Hepatic methylation damage may play a role in the pathophysiology of depression, as evidenced by the first discovery of the abnormality of hepatic methionine metabolism. Abnormal changes in hepatic bile acids may provide stronger evidence for depression pathogenesis involving the microbiota–gut–brain axis, suggesting that the liver is involved in depression development and may be a treatment target. The quercetin treatment alleviated the CUMS-induced liver metabolism disorder, suggesting that quercetin may protect against depression by regulating liver metabolism.

更新日期：2023-01-18

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