• Guo Liu, Ye-Hui Wang, Ting Zhang, Ya-Qiong Li, Xin-Yue Chen, Wei Dong, Wei Li, Qi-Xiang Miao, Wen-Bo Qiao, Hui-Qiang Tian, and Shi-Long Yin.
• Qionglai Hospital of Traditional Chinese Medicine, Qionglai, Chengdu, Sichuan, China.
• Medicine (Baltimore). 2024 Apr 19; 103 (16): e37846e37846.

AbstractThe current study aimed to investigate the potential role of astragaloside IV (AS-IV) in improving cellular lipid deposition and its underlying mechanism. A fatty liver cell model was established by treating hepatoma cells with palmitic acid. AS-IV and SC79 were used for treatment. Oil Red O staining was applied to detect intracellular lipid deposition, and transmission electron microscopy was utilized to assess autophagosome formation. Immunofluorescence double staining was applied to determine microtubule-associated proteins 1A/1B light chain 3 (LC3) expression. Western blot analysis was performed to detect the expression of LC3, prostacyclin, Beclin-1, V-akt murine thymoma viral oncogene homolog (Akt), phosphorylated Akt, mTOR, and phosphorylated mTOR. Oil Red O staining revealed that AS-IV reduced intracellular lipid accumulation. Further, it increased autophagosome synthesis and the expression of autophagy proteins LC3 and Beclin-1 in the cells. It also reduced the phosphorylation levels of Akt and mTOR and the levels of prostacyclin. However, the effects of AS-IV decreased with SC79 treatment. In addition, LC3B + BODIPY493/503 fluorescence double staining showed that AS-IV reduced intracellular lipid deposition levels by enhancing autophagy. AS-IV can reduce lipid aggregation in fatty liver cells, which can be related to enhanced hepatocyte autophagy by inhibiting the Akt/mTOR signaling pathway.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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