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Aloesin improves metabolic associated fatty liver disease and obesity by targeting TGFBR1
Зохиогч
Wu, Jianfeng
Liu, Siqi
Ma, Zhen
Liao, Qichao
Wei, Yutian
Xiao, Yang
Wang, Yang
Chen, Ruxue
Batsaikhan, Batbold
Zhou, Lei
Li, Yixing
Он
2026 оны дөрөвдүгээр сар
Төрөл
journal article
Journal
Phytomedicine : international journal of phytotherapy and phytopharmacology
Volume
153
Start Page
157922
ISSN
1618-095X
Хураангуй
BACKGROUND: Metabolic associated fatty liver disease (MAFLD) is a chronic liver condition with a high global prevalence. Obesity and its associated insulin resistance are among the main risk factors for MAFLD, for which no effective clinical treatments are currently available. Aloesin, a natural chromone compound derived from Aloe vera, has anti-inflammatory, antioxidant, anticancer, and antidiabetes activity. However, its involvement in MAFLD has not been systematically studied.
PURPOSE: This study investigated the effectiveness of aloesin against MAFLD and obesity and elucidated its potential molecular mechanism.
METHODS: Aloesin was added to the high-fat diet-of an induced mouse model and to oleic acid/palmitic acid-induced HepG2 cells to explore its effect on lipid metabolism. Molecular targets were identified by reverse docking, cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS).
RESULTS: Aloesin significantly reduced lipid accumulation in hepatocytes in both the high-fat diet-induced MAFLD mouse model and the oleic acid/palmitic acid-induced HepG2 cells. It also alleviated oxidative stress and energy metabolism disorders and decreased the body fat mass in mice fed the high-fat diet, which ameliorated the pathological features of MAFLD and obesity. Target prediction and validation identified TGFBR1 as a direct target of aloesin, which was confirmed by CETSA and DARTS. Functional experiments demonstrated that overexpression of TGFBR1 increased lipid accumulation and metabolic disturbances, which were reversed by aloesin.
CONCLUSION: Aloesin improved lipid deposition and slowed the progression of MAFLD by targeting TGFBR1. The results support its potential application for the prevention and treatment of MAFLD.