Background
Ultraviolet B (UVB) has been reported to prevent bone loss by promoting the synthesis of vitamin D. However, UVB can also enhance osteoclastic differentiation, inhibit osteogenic differentiation, and cause oxidative damage. The present study aimed to analyze the osteoprotective effects of UVB and conjugated linoleic acid (CLA) in rats with ovariectomy-induced osteoporosis, and to determine the interactions between UVB and CLA and their effects on bone mesenchymal stem cells (BMSCs) and bone marrow mononuclear cells (BMMCs).
Conclusions
CLA can effectively weaken osteoclast promotion, osteogenic inhibition, and oxidative damage caused by UVB. Combination treatment of UVB and CLA exerts an osteoprotective effect on ovariectomized osteoporotic rats and stimulates osteogenesis. The molecular mechanism of this interaction requires further investigation.
Methods
In vitro, the distance of UVB irradiation and the dose of CLA were selected by immunofluorescence assays and Cytotoxicity assay. BMSCs and BMMCs were detected by immunohistochemical and immunofluorescence assays. In vivo, three-month-old female Sprague-Dawley rats that had undergone ovariectomy were treated with UVB and CLA. After 8 weeks of therapy, the femurs of the rats were examined by micro-computed tomography (CT) and immunohistochemical detection to assess the therapeutic efficacy.
Results
The least inhibitive UVB distance and dosage of CLA were selected for the in vivo experiments. CLA effectively weakened the osteogenic inhibitory effect of UVB (72 cm), significantly improved the activity of alkaline phosphatase (ALP), promoted the formation of mineralized nodules, and alleviated the oxidative damage induced by UVB. CLA also effectively weakened the osteoclast-promoting effect of UVB (72 cm), inhibited osteoclast formation, and inhibited the inflammatory damage to BMMCs caused by UVB (72 cm) irradiation. Micro-CT results showed that UVB irradiation could promote bone formation in ovariectomized Sprague-Dawley rats, while CLA could significantly promote bone regeneration. Immunofluorescence assays results showed that CLA alleviated UVB-induced oxidative damage to osteoblasts. The ROS detection results demonstrated that CLA effectively alleviated UVB-induced oxidative damage to BMSCs. Furthermore, Immunohistochemical assays showed that UVB and CLA treatment increased bone density, inhibited osteolytic osteolysis, and enhanced osteogenic activity. Conclusions: CLA can effectively weaken osteoclast promotion, osteogenic inhibition, and oxidative damage caused by UVB. Combination treatment of UVB and CLA exerts an osteoprotective effect on ovariectomized osteoporotic rats and stimulates osteogenesis. The molecular mechanism of this interaction requires further investigation.