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Abstract
Because of the reduced potential for osteogenesis in aging bone marrow stromal cells, the balance of bone metabolism becomes disrupted, leading to various bone diseases. An increase in reactive oxygen species has been determined to be one of the key factors that accelerates the aging process in BMSCs. In these cells, increased expression of NADPH oxidases is the major source of ROS. In the current study, we suppressed the expression of NOX using apocynin, an effective antioxidant and free radical scavenger, and the results showed that aging BMSCs exhibited an enhanced potential for osteogenesis. The expression of potential key targets influencing this reversal was evaluated using qRT-PCR, and the expression of p53 was shown to be reduced with the suppression of NOX. We speculate that this may be one of the major reasons for the reversal of the aging process. We also examined the effect of apocynin in vivo, and the results showed that in SAMP6 mice, bone mineral density and total bone volume were increased after 3 months of apocynin treatment. In conclusion, our results demonstrate that in aging BMSCs, suppression of NADPH oxidase by apocynin partially reverses the aging process and enhances osteogenic potential.
Highlights
Bone marrow stromal cells (BMSCs) play a key role in maintaining the balance of bone metabolism[1,2,3]
The results showed that there was a higher percentage of SA-β –gal-positive cells among the BMSCs isolated from the 22-month-old SD rats than in the control cells isolated from the 4-week-old SD rats (50.55 ± 1.22% vs. 3.10 ± 1.05%) (Fig. S1A)
This result indicated that the BMSCs isolated from the 22-month-old SD rats met the standard of aging cells and could be used as aging BMSCs in the following experiments
Summary
Bone marrow stromal cells (BMSCs) play a key role in maintaining the balance of bone metabolism[1,2,3]. BMSCs become senescent, and their potential for osteogenesis is reduced[5], leading to an imbalance in bone metabolism and resulting in various bone diseases related to aging[6]. Many reports have indicated that apocynin does not inhibit the activity of NADPH oxidase or even up-regulate the expression of ROS in many cell models[17,18,19]. We report for the first time that in a senescent cell model and in mesenchymal stem cells, apocynin suppresses NADPH oxidase and reduces intracellular ROS. Based on these findings, the data showed that the aging process in BMSCs was partially reversed and the osteogenesis potential of the BMSCs was enhanced. We evaluated the effect of apocynin in a mouse model, and the results demonstrated that the potential for osteogenesis was increased, while the ROS level was decreased
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