Marine derivative CHNQD-00603 reverses bone marrow mesenchymal stem cells senescence by enhancing autophagy through the AKT/ERK/mTOR signaling pathway

Objective Maxillofacial bone defect caused by the tumor and periodontal disease in the elderly will affect implant restoration. Bone marrow mesenchymal stem cells (BMSCs), as seed cells for bone regeneration, play an important role in the treatment of bone defects. The objective of this study was to investigate the effect and mechanism of marine derivative CHNQD-00603 on senescence BMSCs. Materials and Methods Biological function of BMSCs was determined by flow cytometry, alizarin red and oil-red O. Transmission electron microscopy Western blot, qRT-PCR, and reactive oxygen species detection were used to evaluate the effects of CHNQD-00603 on autophagosomes, autophagy-related molecules, senescence-related indicators, and ROS in aging BMSCs. The mechanism of CHNQD-00603 inhibiting BMSCs aging was detected by Western blot and qRT-PCR. Results In this study, CHNQD-00603 increased the level of autophagy, and decreased the level of ROS in senescence BMSCs. In addition, CHNQD-OO603 decreased AKT/ERK phosphorylation and increased mTOR phosphorylation. The agonists of AKT and ERK can increase the mRNA expression of age-related genes p16 and p21. Conclusions Our findings revealed that CHNQD-OO603 inhibits BMSCs senescence via the AKT/ERK/mTOR signaling pathway. This provides a potential idea for the treatment of insufficient jaw volume in the elderly.