Chemical Constituents of Halophyte Suaeda glauca and Their Anti-Adipogenic and Anti-Inflammatory Activities

Halophytes are recognized as rich sources of secondary metabolites with a wide range of biological activities. To explore the phytochemical constituents and biological activities of Korean halophytes, we investigated Suaeda glauca, a salt-tolerant species belonging to the family Amaranthaceae. In traditional Chinese medicine, S. glauca has been used to reduce fever and alleviate food retention, and it has also been consumed as a food source. In the present study, we conducted a phytochemical investigation of the aerial parts of S. glauca. Column chromatographic separation of the CH2Cl2-soluble fraction of its hot-water extract, followed by high-performance liquid chromatography (HPLC) purification, resulted in the isolation of six compounds (1–6). Their structures were identified as vanillin (1), syringaldehyde (2), (–)-loliolide (3), N-trans-feruloyltyramine (4), N-trans-feruloylmethoxytyramine (5), and (–)-syringaresinol (6) through spectroscopic analyses and comparison with previously reported data. Notably, this study represents the first report of compounds 1–3 and 6 being isolated from S. glauca. The isolated compounds were evaluated for their anti-adipogenic and anti-inflammatory activities using 3T3-L1 adipocytes and TNF-α-stimulated AGS cells, respectively. Compound 2 suppressed adipocyte differentiation, accompanied by reduced lipid accumulation and decreased expression of PPARγ, C/EBPα, and adiponectin, whereas compound 6 attenuated TNF-α-induced inflammatory responses by reducing IL-8 production and ERK/p38 MAPK activation. To conceptualize these biological effects, computational network pharmacology and molecular docking were employed, identifying PTGS2 (COX-2) as a theoretical mechanistic bridge linking the PPARγ metabolic axis and the MAPK inflammatory cascade. Collectively, these findings expand the phytochemical knowledge of S. glauca and provide structurally supported hypothesis for the dual-axis modulation of metaflammation by its major active constituents.