Suppression of adipogenesis by Hydrangea serrata extract via inhibition of mTOR signaling and cytoskeletal remodeling
摘要
This study examined the anti-obesity effects of Hydrangea serrata extract (HE) by analyzing its effects on adipocyte differentiation, lipid accumulation, and mechanistic target of rapamycin (mTOR) signaling. To evaluate its bioactivity, its secondary metabolites and antioxidant capacity were assessed. HE contained 35.2 mg of gallic acid equivalents per gram of dry matter (DM) of total polyphenols and 11.0 mg quercetin equivalents per gram of DM of total flavonoids, with 2,2-diphenyl-1-picrylhydrazyl and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging activities of 84.4% and 76.2%, respectively. In the evaluation of triglyceride accumulation, HE (0.25 mg/mL) significantly reduced lipid droplet formation by 12.5% to 50.1% (p < 0.05), indicating an inhibitory effect on adipogenesis. Gene expression analysis revealed reductions ranging from 31.7 to 35.0% in adipocyte differentiation-related factors (C/EBP-α, C/EBP-β, and PPAR-γ). Lipid synthesis-related factors (SREBP-1c, FAS, and mTOR) were downregulated by 30.3% to 35.0% (p < 0.05). Protein expression analysis confirmed these findings, showing reductions of 32.8% to 46.7% in adipogenesis factors and a 16.0% to 46.2% reduction in lipid synthesis factors. Immunofluorescence analysis revealed that HE treatment inhibited adipogenic differentiation in 3T3-L1 cells by reduction in fluorescence intensity of DAPI by 44.1%, Mitotracker by 68.3% and increased F-actin by 47.5%, preserving nuclear integrity, suppressing mitochondrial activity, and stabilizing the actin cytoskeleton. These findings demonstrate that HE effectively suppresses adipogenesis and lipid accumulation, supporting its potential as a bioactive functional ingredient for obesity prevention and metabolic health improvement.