[1]吴海滨,林基伟,宋晓容,等.基于PI3K/AKT/Foxo1信号通路探讨大黄素防治非酒精性脂肪肝的作用机制[J].西部中医药,2025,38(07):18-23.[doi:10.12174/j.issn.2096-9600.2025.07.04]
　WU Haibin,LIN Jiwei,SONG Xiaorong,et al.Emodin Prevents and Treats NAFLD via PI3K/AKT/Foxol Signaling Pathway[J].Western Journal of Traditional Chinese Medicine,2025,38(07):18-23.[doi:10.12174/j.issn.2096-9600.2025.07.04]
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基于PI3K/AKT/Foxo1信号通路探讨大黄素防治非酒精性脂肪肝的作用机制()

《西部中医药》[ISSN:2096-9600/CN:62-1204/R]

卷:
38
期数:
2025年07期
页码:
18-23
栏目:
基础研究
出版日期:
2025-07-15

文章信息/Info

Title:
Emodin Prevents and Treats NAFLD via PI3K/AKT/Foxol Signaling Pathway
作者:
吴海滨1, 林基伟1, 宋晓容1, 程波敏1, 刘卓超1, 朱艳萍1, 谭梅傲1,2
1.深圳市中医院治未病中心，广东 深圳 518033
2.重庆市中医院，重庆 404121
Author(s):
WU Haibin1, LIN Jiwei1, SONG Xiaorong1, CHENG Bomin1, LIU Zhuochao1, ZHU Yanping1, TAN Meiao1,2
1.Preventive Medicine Center, Shenzhen Hospital of TCM, Shenzhen 518033, China
2.Chongqing Hospital of TCM, Chongqing 404121, China
关键词:
脂肪性肝; 非酒精性; 大黄素; 甘油三酯; 总磷脂酰肌醇3-激酶; 蛋白激酶B; 叉头框蛋白1; 甘油三酯转运蛋白; 载脂蛋白CⅢ
Keywords:
fatty liver disease;  nonalcoholic; emodin; triglyceride; phosphatidylinositol 3-kinase; RAC-beta serine/threonine-protein kinase; forkhead box; triglyceride transport protein; apolipoprotein
分类号:
R25
DOI:
10.12174/j.issn.2096-9600.2025.07.04
文献标志码:
A
摘要:
目的探讨大黄素改善油酸+棕榈酸诱导非酒精性脂肪肝（nonalcoholic fatty liver di-sease，NAFLD）脂质堆积模型的机制。 方法利用网络药理学预测大黄素干预NAFLD的信号通路；在体外利用油酸+棕榈酸模拟NAFLD的体外模型，15、30 μM大黄素干预NAFLD体外模型48 h，检测细胞内甘油三酯（triglycerides，TG）含量，油红染色评价细胞脂质堆积情况，蛋白质免疫印迹（western blot，WB）检测总磷脂酰肌醇3-激酶（Phosphatidylinositol 3-kinase，PI3K）、蛋白激酶Bβ（RAC-beta serine/threonine-protein kinase，AKT2）、磷酸化叉头框蛋白1（Phospho-forkhead box，pFoxo1）/叉头框蛋白1（forkhead box，Foxo1）及核pFoxo1/Foxo1，实时荧光定量PCR检测PI3K、AKT2、Foxo1、微粒体甘油三酯转运蛋白、载脂蛋白CⅢ（Apolipoprotein，apoC-Ⅲ）的表达。 结果网络药理学预测大黄素共得到34个靶点，这些靶点显著富集在胰岛素抵抗、PI3K/AKT/Foxo1信号通路中。15、30 μM大黄素干预的细胞内TG含量减少；大黄素能改善油酸+棕榈酸诱导BRL细胞的脂质堆积；30 μM大黄素可显著上调模型组总PI3K、AKT，下调pFoxo1/Foxo1；30 μM大黄素组可下调模型组MTTP、apoC-Ⅲ的表达。 结论大黄素可能通过调节PI3K/AKT/Foxo1降低脂质的堆积。
Abstract:
ObjectiveTo investigate the mechanism of emodin in improving lipid accumulation model with NAFLD induced by oleic acid+palmic acid. MethodsNetwork pharmacology was utilized to predict emodin in the intervention of the signaling pathway of NAFLD; the in-vitro models of NAFLD were simulated using oleic acid+palmic acid, and intervened with 15 and 30 μM of emodin for 48 hours, to detect the contents of TG, oil red O (ORO) staining was used to assess cell lipid accumulation, WB was applied to measure PI3K, AKT2, pFoxo1/Foxo1 and nuclear pFoxo1/Foxo1, real-time quantitative PCR was utilized to detect the expressions of PI3K, AKT2, Foxo1, microsomal triglyceride transfer protein and apoC-Ⅲ. ResultsIn total, 34 targets were predicted for emodin by network pharmacology, and these targets were significantly enriched in the signaling pathways such as insulin resistance and PI3K/AKT/Foxol. The contents of TG were lowered in the cells after intervened with 15 and 30 μM of emodin; emodin could improve lipid accumulation in BRL cells induced by oleic acid+palmic acid; 30 μM of emodin could noticeably upregulate the levels of PI3K and AKT of the model group, and downregulate pFoxo1/Foxo1; 30 μM of emodin could lower the expressions of MTTP and apoC-Ⅲ of the model group. ConclusionEmodin could reduce lipid accumulation possibly through adjusting PI3K/AKT/Foxol.

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备注/Memo

备注/Memo:
吴海滨（1987—），男，博士学位，主任医师。研究方向：肝胆代谢性疾病中医药基础临床研究与治未病健康管理。国家自然科学青年基金（82204953）；广东省中医药局科研项目（20211325）；深圳市卫生健康委员会医防融合中医药组项目（深卫健体改〔2019〕25号）；深圳市中医“治未病”重点专科建设项目；成都中医药大学杏林学者科研提升计划（YYZX2021056）；重庆市自然科学基金—博士后项目（CSTB2022NSCQ-BHX0032）。
更新日期/Last Update: 2025-07-15