Abstract
Objectives Flufenamic acid (FFA) is a representative of the fenamic acids, an important group of NSAIDs. In the present study, we study the effects of FFA on adipogenesis of human mesenchymal stem cells (MSCs) and we explore the potential mechanism. Methods To investigate the effects of FFA on adipogenic differentiation of hMSCs, human adipose-derived stem cells (hASCs) and human bone marrow mesenchymal stem cells (hBMMSCs), representative of hMSCs, were treated with FFA during adipogenic differentiation in vitro. The effects of FFA in vivo were evaluated using a heterotopic adipose formation assay in nude mice as well as ovariectomized (OVX) and aged mice. To explore the mechanism of FFA, Western blot was used to determine activation of the PI3K/AKT signaling pathway. Results Our results demonstrate that, at certain concentrations, FFA inhibited adipogenesis of human MSCs both in vitro and in vivo. Mechanistically, FFA inhibited adipogenesis of human MSCs by inhibiting the PI3K/AKT pathway. Conclusions The present study indicated that FFA could be used to inhibit adipogenesis of human MSCs in tissue engineering and diseases related to excessive adipogenic differentiation of MSCs.
Highlights
Tissue engineering has become a hotspot in recent years [1]
We report a potential mechanism of action, which provides valuable insight into the potential use of FFA in tissue engineering and diseases related to excessive adipogenic differentiation of mesenchymal stem cells (MSCs)
The inhibitory effect was attenuated with increasing FFA concentration, and 25 μM FFA showed the strongest inhibitor effect on adipogenic differentiation (Figures 1(a)–1(d))
Summary
Tissue engineering has become a hotspot in recent years [1]. As a commonly used seed cell in tissue engineering, mesenchymal stem cells (MSCs) which have multipotent differentiation potential play an important role [2,3,4,5,6]. Much focus has been placed on how to regulate the lineage commitment of MSCs. Adipogenic differentiation is one of the differentiation direction of MSCs which has important physiological and pathological significance [2, 3]. Excessive adipogenic differentiation of MSCs can be seen in several diseases, such as obesity [7, 8] and osteoporosis [9]. How to regulate the adipogenesis of MSCs has attracted more and more attention
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