Artemisia princeps Inhibits Adipogenic Differentiation of 3T3-L1 Pre-Adipocytes via Downregulation of PPARγ and MAPK Pathways

太子蒿通过下调 PPARγ 和 MAPK 通路抑制 3T3-L1 前脂肪细胞的脂肪形成分化

阅读:13
作者:Jung Hwan Oh, Fatih Karadeniz, Jung Im Lee, Youngwan Seo, Chang-Suk Kong

Abstract

Artemisia princeps, the Korean mugwort, is an edible plant that has various beneficial effects on health, and which has been used as a part of traditional folk medicine. The current study investigated the possible effects of solvent (H2O, n-BuOH, 85% aq. MeOH, and n-hexane) partitioned fractions of A. princeps crude extract (APE) on adipogenic differentiation of 3T3-L1 mouse pre-adipocytes. Characteristics of the differentiated adipocytes were evaluated by Oil red O staining of intracellular lipid droplets, analyzing mRNA and protein levels of peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, and sterol regulatory element-binding protein (SREBP)-1c, and immunoblotting of phosphorylated mitogen-activated protein kinase (MAPK) pathway proteins such as p38, extracellular-signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). Introduction of APE fractions to differentiating adipocytes resulted in lowered lipid accumulation and downregulation of the PPARγ pathway. APE fractions significantly decreased mRNA and protein expression of PPARγ, C/EBPα, and SREBP-1c. Analysis of MAPK pathway activation showed similar results since treatment with the APE fraction treatment decreased levels of phosphorylated p38, ERK, and JNK. Overall, the n-BuOH and n-hexane fractions were observed to be the most active fractions to suppress adipogenesis-related signaling in 3T3-L1 cells. The promising ability of APE fractions to inhibit adipocyte differentiation of 3T3-L1 cells suggest that A. princeps has potential to be utilized as a source of anti-obesity compounds.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。