Chrysanthemum indicum suppresses adipogenesis by inhibiting mitotic clonal expansion in 3T3-L1 preadipocytes.
Won-Ju KimHyung-Seok YuWon-Young BaeKyung Yuk KoKyung-Hoon ChangNa-Kyoung LeeHyun-Dong PaikPublished in: Journal of food biochemistry (2021)
Herbs have been of interest to treat diseases, including obesity, owing to their various bioactive constituents that exhibit therapeutic and prophylactic properties. The present study examined the anti-adipogenic effects and mechanisms of Chrysanthemum indicum aqueous extract (CAE) in 3T3-L1 preadipocytes. CAE comprises 1,3-dicaffeoylquinic acid, chlorogenic acid, kaempferol-3-O-glucoside, caffeic acid, and apigenin, which were corresponded with previous reports. CAE inhibited the accumulation of lipid droplets and significantly alleviated the expression of lipogenesis- and adipogenesis-associated biomarkers. Treatment with CAE inhibited the mitotic clonal expansion (MCE), corroborated by cell cycle arrest at the G0 /G1 phase, and mitigated the expression of cell cycle progression-associated proteins and in addition to phosphorylation of MCE-promoting transcription factors. Moreover, CAE downregulated the activation of Akt and extracellular signal-regulated kinase 1/2 signaling pathways. In summary, CAE facilitates adipogenic inhibition during the early phase of differentiation, especially MCE, and its phenolic compounds can contribute to its anti-obesogenic properties. PRACTICAL APPLICATIONS: Chrysanthemum indicum has been mainly used as traditional herbal tea and drinks. Chrysanthemum indicum aqueous extract (CAE) inhibits adipogenesis by suppressing mitotic clonal expansion during the early phase of differentiation in 3T3-L1 preadipocytes. 1,3-Dicaffeoylquinic acid, chlorogenic acid, kaempferol-3-O-glucoside, caffeic acid, and apigenin were detected in CAE. Based on these findings, CAE can be used as nutraceutical agents for prevention and treatment of obesity.
Keyphrases
- anti inflammatory
- cell cycle
- signaling pathway
- high fat diet induced
- cell proliferation
- insulin resistance
- type diabetes
- poor prognosis
- metabolic syndrome
- transcription factor
- weight loss
- pi k akt
- emergency department
- cell death
- physical activity
- binding protein
- protein kinase
- weight gain
- skeletal muscle
- oxidative stress