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3-Acetyl-11-Keto-Beta-Boswellic Acid Inhibits Adipogenesis by Suppressing Autophagy and Inducing AMPK Phosphorylation
Faizullah Khan1,2, Muhammad Waqas1, Hassan Moghtaderi1
1Natural and Medical Sciences Research Center, University of Nizwa, Nizwa 616, Oman.
Background/Aims:
Adipogenesis involves preadipocyte differentiation and lipid droplet accumulation and is closely linked to obesity. 3-Acetyl-11-keto-beta-boswellic acid (AKBA), a frankincense-derived triterpene, has anti-inflammatory and anticancer properties, but its role in adipocyte differentiation remains unclear.
Methods:
3T3-L1 preadipocytes were induced to differentiate with or without varying concentrations of AKBA. Cell viability was assessed by MTT assay, lipid accumulation by Oil Red O staining, and apoptosis by annexin V-FITC assay. Expression of adipogenic transcription factors, lipid-associated proteins, apoptotic markers, autophagy-related proteins, and AMPK phosphorylation was analysed by Western blotting. Molecular docking was used to evaluate AKBA interactions with target proteins.
Results:
AKBA inhibited adipocyte differentiation by suppressing C/EBPβ, C/EBPα, and PPARγ expression, reduced lipid accumulation, increased apoptosis via an elevated Bax/Bcl2 ratio, suppressed autophagy markers ATG5 and LC3b, and enhanced AMPK phosphorylation. Docking studies suggested AKBA binding to PPARγ and ATG5.
Conclusion:
AKBA suppresses adipogenesis by inhibiting adipogenic transcription factors, autophagy, and activating AMPK, supporting its potential as an anti-obesity therapeutic candidate.
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