为证实这一假说，LDL受体基因敲除小鼠拟议被应用以建立高脂血症骨损伤模

To confirm this hypothesis, LDL receptor gene knockout mice are proposed to be used to establish a hyperlipidemia bone injury model, and methods such as transcriptomics and bioinformatics analysis are used to focus on the role of sEH in angiogenesis and osteogenesis. Action and mechanism, clarify the effect of epoxide hydrolase on bone injury in hyperlipidemia mice, evaluate the effect and transformation prospects of sEH inhibitors on hyperlipidemia-related bone diseases, and clarify that sEH regulates bone angiogenesis Molecular mechanism.

To support this hypothesis, LDL-subject gene knock-out mice are proposed to be used to build models of hyperlipidemia bone injury, and transcriptometology and bioinfossion are used around the role and mechanism of sEH in angiogenesic and bone production To clarify the effects of cyclooxid hydrolyzedase on bone injury in mice with hyperlipidemia, to evaluate the effect and transformation prospects of sEH inhibitors on the treatment of hyperlipidemia-related osteopathy, and to clarify the molecular mechanism of sEH controlling bone angiogenesy.

In order to confirm this hypothesis, LDL receptor knockout mice are proposed to be used to establish a hyperlipidemic bone injury model, and transcriptomics and bioinformatics methods are used to analyze the role and mechanism of sEH in angiogenesis and osteogenesis, clarify the effect of epoxide hydrolase on bone injury in hyperlipidemic mice, and evaluate the effects of sEH inhibitors on hyperlipidemic related bone diseases To elucidate the molecular mechanism of sEH regulating femoral angiogenesis.<br>