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齐墩果酸通过调节高脂饮食喂养小鼠的脂质代谢来减轻肥胖。

Oleanolic acid attenuates obesity through modulating the lipid metabolism in high-fat diet-fed mice.

作者信息

Zhang Guangjie, Zhang Huiying, Dong Ruiyi, Zhao Hongmei, Li Junfeng, Yue Weiming, Ma Zheng

机构信息

School of Biology and Food Engineering Anyang Institute of Technology Anyang China.

Department of Thoracic Surgery Qilu Hospital of Shandong University Jinan China.

出版信息

Food Sci Nutr. 2024 Aug 29;12(10):8243-8254. doi: 10.1002/fsn3.4408. eCollection 2024 Oct.

Abstract

As a natural pentacyclic triterpenoid, oleanolic acid has hepatoprotective, anti-inflammatory, and antioxidant activities. This work performed the in vitro experiments and animal assay to explore whether oleanolic acid alleviates lipid accumulation induced by high-fat diet by mediating PPARγ. Oil red O staining showed that oleanolic acid can reduce lipid accumulation in HepG2 cells, which were treated with oleic acid and palmitic acid. Immunofluorescence, western blot analysis, and RT-qPCR showed that oleanolic acid could promote nuclear translocation of PPARγ and reduce the expression level of PPARγ, C/EBP-β, and SREBP-1c. The results of in vivo experiments indicated that dietary intervention with oleanolic acid can effectively improve the fat accumulation in liver tissue and attenuate the level of IL-6 and TNF-α in serum caused by high-fat diet. Meanwhile, oleanolic acid did not cause lesions in vital organs at the experimental concentrations. In addition, the computer simulation indicated that oleanolic acid could directly bind to PPARγ with a reasonable and stable docking conformation. The above research results can provide new evidence for oleanolic acid to prevent nonalcoholic fatty liver disease.

摘要

作为一种天然的五环三萜类化合物,齐墩果酸具有保肝、抗炎和抗氧化活性。本研究通过体外实验和动物实验,探讨齐墩果酸是否通过介导过氧化物酶体增殖物激活受体γ(PPARγ)来减轻高脂饮食诱导的脂质积累。油红O染色显示,齐墩果酸可减少经油酸和棕榈酸处理的HepG2细胞中的脂质积累。免疫荧光、蛋白质免疫印迹分析和实时定量聚合酶链反应表明,齐墩果酸可促进PPARγ的核转位,并降低PPARγ、C/EBP-β和SREBP-1c的表达水平。体内实验结果表明,齐墩果酸饮食干预可有效改善肝脏组织中的脂肪积累,并减轻高脂饮食引起的血清中白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平。同时,在实验浓度下,齐墩果酸未对重要器官造成损伤。此外,计算机模拟表明,齐墩果酸能够以合理且稳定的对接构象直接与PPARγ结合。上述研究结果可为齐墩果酸预防非酒精性脂肪性肝病提供新的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cbe/11521747/ef86b9206bfa/FSN3-12-8243-g001.jpg

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