Abstract
Luteolin is a common phytochemical from the flavonoid family with a flavone structure. Studies reported several bioactivities for luteolin and similar flavones. Attenuating the increased adipogenesis of bone marrow cells (hBM-MSCs) has been regarded as a therapeutic target against osteoporotic bone disorders. In the present study, the potential roles of luteolin and its sulfonic acid derivative luteolin-OSO3Na in regulating adipogenic differentiation of hBM-MSCs were investigated. Adipo-induced cells were treated with or without compounds, and their effect on adipogenesis was evaluated by adipogenic marker levels such as lipid accumulation and PPARγ pathway activation. Luteolin hindered the adipogenic lipid accumulation in adipo-induced hBM-MSCs. Immunoblotting and reverse transcription-polymerase chain reaction analysis results indicated that luteolin downregulated PPARγ and downstream factors of C/EBPα and SREBP1c expression which resulted in inhibition of adipogenesis. Luteolin-OSO3Na showed similar effects; however, it was significantly less effective compared to luteolin. Investigating p38, JNK, and ERK MAPKs and AMPK activation indicated that luteolin suppressed the MAPK phosphorylation while stimulating AMPK phosphorylation. On the other hand, luteolin-OSO3Na was not able to notably affect the MAPK and AMPK activation. In conclusion, this study suggested that luteolin inhibited adipogenic differentiation of hBM-MSCs via upregulating AMPK activation. Replacing its 4′-hydroxyl group with sulfonic acid sodium salt diminished its antiadipogenic effect indicating its role in regulating AMPK activation. The general significance is that luteolin is a common phytochemical with various health-beneficial effects. The current study suggested that luteolin may serve as a lead compound for developing antiosteoporotic substances with antiadipogenic properties.
Highlights
Obesity is a worldwide health problem, and many diseases such as cardiovascular disease, liver and kidney diseases, diabetes, and cancer are considered to be linked with the prior cases of excess body fat accumulation [1]
Obesity development occurs through high rates of proliferation and differentiation of white adipocytes, which result in expanding white adipose tissue
Studies have shown that luteolin inhibited the adipogenic differentiation of mouse preadipocyte cells [11] as well as inducing browning and thermogenesis in mice adipose tissue [12]
Summary
Obesity is a worldwide health problem, and many diseases such as cardiovascular disease, liver and kidney diseases, diabetes, and cancer are considered to be linked with the prior cases of excess body fat accumulation [1]. In addition to adipocyte differentiation in adipose tissue itself, obesity-linked complications are known to meditate the other. It was showed that mesenchymal stromal cells of other organs such as bone marrow can play roles in adipose tissue homeostasis through adipogenic differentiation [4]. Cultured human bone marrow-derived mesenchymal stromal cells (hBMMSCs), are reliable and well-known in vitro models for studying human adipogenesis mechanisms and ways to hinder it. Studies have shown that luteolin inhibited the adipogenic differentiation of mouse preadipocyte cells [11] as well as inducing browning and thermogenesis in mice adipose tissue [12]. Erefore, the current study was aimed to investigate the possible antiadipogenic properties and underlying mechanisms of luteolin and its sulfate derivative, luteolin-4′-sulfonate, using adipogenesis-induced human bone marrow-derived mesenchymal stem cells (hBMMSCs)
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