Evaluation of the osteogenic effect of apigenin on human mesenchymal stem cells by inhibiting inflammation through modulation of NF-κB/IκBα

Abstract

Background and purpose: Apigenin has stimulatory effects on osteogenic differentiation of human mesenchymal stem cells (hMSCs) as well as anti-inflammatory properties. This study investigated the osteogenic differentiation of hMSCs in inflammatory conditions treated with apigenin focusing on nuclear factor kappa-light-chain-enhancer of activated B (NF-кB), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) and nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3) inflammatory pathways. Experimental approach: Along with osteogenic differentiation of the hMSCs, they became inflamed with lipopolysaccharide (LPS)/palmitic acid (PA) and treated with apigenin. Alizarin red staining, alkaline phosphatase (ALP) activity, and Runt-related transcription factor 2 (RUNX2) gene expression were used to determine the degree of differentiation. Also, gene expression of NLRP3 was performed along with protein expression of interleukin 1-beta (IL-1β), NF-кB, and IκBα. Findings / Results: Apigenin was shown to be effective in neutralizing the inhibitory impact of LPS/PA on osteogenesis. Apigenin increased MSC osteogenic capacity by inhibiting NLRP3 expression and the activity of caspase-1. It was also associated with a considerable decrease in the protein expression of NF-κB and IκBα, as well as IL-1β, in these cells. Conclusion and implications: The effects of apigenin on osteogenesis under inflammatory conditions were cautiously observed.

P65 mediated UBR4 in exosomes derived from menstrual blood stromal cells to reduce endometrial fibrosis by regulating YAP Ubiquitination

“…Similarly, the NF-κB signaling pathway also exerted a regulatory effect on human mesenchymal stem cells. A study by Azita Asadi et al found that apigenin could restore the osteogenic differentiation of adipose stem cells in an inflammatory environment by regulating the expression of some key factors in the NF-κB signaling pathway [ 53 ]. In hematopoietic stem cells, the NF-κB signaling pathway was activated, which enhanced the survival and function of hematopoietic stem cells, to promote the recovery of myeloid differentiation function and hematopoietic function [ 37 ] We also predicted that P65, a transcription factor in the NF-κB family, could bind to the UBR4 promoter region, thus we hypothesized that P65 could promote the expression of UBR4 in MenSCs.…”