| Objective To explore the effect of allicin on bone metabolism in atherosclerotic mice and its potential mechanism of action. Methods After 8 weeks of feeding with a high-fat diet, SPF-grade male ApoE?/? mice were grouped using a random grouping method, with 8 mice in each group, including the model group, the allicin group, and the atorvastatin group. Mice were administered drugs continuously for 9 weeks. In addition, 8 C57BL/6N wild-type mice were taken as the control group and fed with a regular diet routinely. Biochemical methods were used to determine the serum lipid levels in mice, including serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). ELISA were used to determine the changes in serum bone resorption markers, including TRAP and CTX-1. Meanwhile, micro-CT was used to scan the bone microstructure of mice. Fourier transform infrared spectroscopy was applied to detect bone material properties. HE staining and TRAP staining were performed to observe the pathological structure of bone tissue. Western blotting was used to detect the expression levels of bone resorption-related proteins (NFATc1, c-Fos, Cathepsin K) and proteins related to the PPARγ/ERRα/PGC-1β pathway in the bone tissue. Results Allicin intervention significantly reduced the serum levels of TG, TC, HDL-C, and LDL-C in atherosclerotic mice, while inhibiting the destruction of bone microstructure, improving bone material properties, and alleviating the pathological damage of bone tissue. In addition, allicin down-regulated the serum levels of TRAP and CTX-1 in atherosclerotic mice, decreased the expressions of NFATc1, c-Fos, and Cathepsin K proteins in the bone tissue, and inhibited the expressions of PPARγ, ERRα, and PGC-1β proteins. Conclusion Allicin improves bone quality in atherosclerotic mice by inhibiting the PPARγ/ERRα/PGC-1β pathway, thereby preventing and treating the occurrence and development of osteoporosis. |