Abstract
BackgroundOsteoporosis is a common disease closely associated with aging. In this study, we aimed to investigate the role of Cornuside I in promoting osteogenic differentiation of bone mesenchymal stem cells (BMSCs) and the potential mechanism.MethodsBMSCs were isolated and treated with different concentrations of Cornuside I (0, 10, 30, 60 μM). Cell proliferation was analyzed by Cell Counting Kit-8 (CCK-8) assay. RNA sequencing was performed on the isolated BMSCs with control and Cornuside I treatment. Differentially expressed genes were obtained by the R software. Alkaline phosphatase (ALP) staining and Alizarin Red Staining (ARS) were performed to assess the osteogenic capacity of the NEO. qRT-PCR and western blot were used to detect the expression of osteoblast markers.ResultsCornuside I treatment significantly improved BMSC proliferation. The optimal dose of Cornuside I was 30 μM (P < 0.05). Cornuside I dose dependently increased the ALP activity and calcium deposition than control group (P < 0.05). A total of 704 differentially expressed genes were identified between Cornuside I and normal BMSCs. Cornuside I significantly increased the PI3K and Akt expression. Moreover, the promotion effects of Cornuside I on osteogenic differentiation of BMSCs were partially blocked by PI3K/Akt inhibitor, LY294002.ConclusionCornuside I plays a positive role in promoting osteogenic differentiation of BMSCs, which was related with activation of PI3K/Akt signaling pathway.
Highlights
Osteoporosis is a common disease closely associated with aging
Identified differentially expressed miRNAs between OA and normal samples To analyze the differentially expressed mRNAs between normal and Cornuside I-treated bone mesenchymal stem cells (BMSCs), RNA sequencing profile was subjected to bioinformatic analysis
A total of 704 differentially expressed genes were identified between Cornuside I and normal BMSCs
Summary
We aimed to investigate the role of Cornuside I in promoting osteogenic differentiation of bone mesenchymal stem cells (BMSCs) and the potential mechanism. Osteoporosis (OP) is a systemic metabolic bone disease caused by decreased bone density and bone mass [1, 2]. Bone formation is a developmental process involving the differentiation of mesenchymal stem cells (MSCs) into osteoblasts [9]. The decreased ability of osteogenic potential of osteoblasts from MSCs is the major risk of OP [10]. Promoting osteogenic differentiation is an important strategy to enhance bone mineral density and slow the development of OP [11]. Other clinical drug treatments for osteoporosis mainly include bone resorption inhibitors such as bisphosphonates and
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