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苦瓜中的皂苷通过诱导自噬减少HepG2细胞系中的脂质积累。

Saponins from bitter melon reduce lipid accumulation via induction of autophagy in and HepG2 cell line.

作者信息

Bai Juan, Zhu Ying, He Linzhao, Zhang Jinfu, Li Jie, Pan Ruirong, Zhang Jiayan, Zhao Yansheng, Cui Lin, Lu Haina, Jiang Ya, Xiao Xiang

机构信息

School of Food and Biological Engineering, Jiangsu University, Zhenjiang, 212013, China.

Jiangsu Jiangnan Biotechnology Co. LTD, Zhenjiang, 212013, China.

出版信息

Curr Res Food Sci. 2022 Jul 22;5:1167-1175. doi: 10.1016/j.crfs.2022.06.011. eCollection 2022.

DOI:10.1016/j.crfs.2022.06.011
PMID:35936825
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9352806/
Abstract

Saponins from bitter melon (BMS) are well-known to have various biological activities, especially in the field of fat-lowering. However, many gaps remain in our knowledge of BMS-induced fat reduction and health benefits. Here, we aimed to investigate the precise mechanism of BMS in alleviating fat accumulation in and HepG2 cell line. Results indicated that BMS showed strong fat-lowering and lifespan-extension properties. Lipidomic analysis illustrated that BMS could alter the lipid profile, especially represented by phosphatidylethanolamine (PE) increase, which plays an essential role in autophagy. Furthermore, we applied gene-deficient mutants and RNAi technology to confirm that BMS largely depended on /FoxO1 and 30/TFEB mediated lipophagy to reduce fat deposition. In addition, BMS could ameliorate oil acid (OA)-induced fat accumulation in HepG2 cells by induction of autophagy-related proteins, such as the phosphorylated AMPK and LC3B. In conclusion, our results elucidated the underlying mechanism of bitter melon saponins interfering with lipid metabolism from the autophagy point of view, which provide new insights into a nutraceutical to mitigate obesity.

摘要

苦瓜皂苷(BMS)以具有多种生物活性而闻名,尤其是在降脂领域。然而,我们对BMS诱导的减脂作用及其健康益处的了解仍存在许多空白。在此,我们旨在研究BMS减轻脂肪积累的精确机制,研究对象为 细胞系和HepG2细胞系。结果表明,BMS具有很强的降脂和延长寿命的特性。脂质组学分析表明,BMS可以改变脂质谱,尤其是以磷脂酰乙醇胺(PE)增加为代表,而PE在自噬中起重要作用。此外,我们应用基因缺陷突变体和RNA干扰技术证实,BMS在很大程度上依赖于 /FoxO1和30/TFEB介导的脂肪自噬来减少脂肪沉积。此外,BMS可以通过诱导自噬相关蛋白(如磷酸化的AMPK和LC3B)来改善油酸(OA)诱导的HepG2细胞脂肪积累。总之,我们的研究结果从自噬角度阐明了苦瓜皂苷干扰脂质代谢的潜在机制,为一种减轻肥胖的营养保健品提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/d9fd2cb6c867/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/5b54eaf6e2aa/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/cdf4ba975644/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/f2e05950d0ae/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/fb1fef02244c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/359d436a290e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/d9fd2cb6c867/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/5b54eaf6e2aa/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/cdf4ba975644/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/f2e05950d0ae/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/fb1fef02244c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/359d436a290e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c01/9352806/d9fd2cb6c867/gr5.jpg

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