关于sEH调控高脂血症LDLR-/-小鼠骨血管生成及骨流失机制的研究可

Research on the mechanism of sEH regulating bone angiogenesis and bone loss in hyperlipidemia LDLR-/- mice. <br><br><br>Soluble epoxide hydrolase (sEH) has attracted much attention in recent years as a therapeutic target for cardiovascular diseases. <br><br>sEH inhibitors, characterized by their broad biological effects such as anti-inflammatory, promoting angiogenesis, lowering blood pressure, and vasodilation, have become a new hot spot in the treatment of metabolic diseases. <br><br>For the first time, our research group discovered that sEH inhibitors can improve early osteoporosis. <br><br>Based on the basis of previous research, we propose that a high-fat diet can induce high expression of sEH, stimulate the activation of osteoclasts, accelerate bone transformation and inflammation, and reduce bone angiogenesis and inhibit bone by regulating the HIF1α/VEGF signal transduction pathway. Formation, so inhibition of sEH can be used for osteoporosis treatment. <br><br>To confirm the hypothesis, the LDL receptor gene is intended to be used in knockout mice to establish a hyperlipidemia bone injury model, and transcriptomics and bioinformatics analysis methods are used to focus on the role of sEH in angiogenesis and osteogenesis. Mechanism, clarify the effect of epoxide hydrolase on bone damage in hyperlipidemia mice, evaluate the effect and transformation prospects of sEH inhibitors on the treatment of hyperlipidemia-related bone diseases, and clarify that sEH regulates bone angiogenesis Molecular mechanism. <br><br>This study was carried out to further provide a reliable molecular basis experimental basis for the pathogenesis of metabolic bone disease, and to open up a new treatment direction for delaying the progress of osteoporosis.

The study on the mechanism of bone angiogenesy and bone loss in mice with sEH regulation of LDLR-/- hyperlipidemia<br><br>Soluble cyclolytic hydrolyzed enzyme (sEH) has been a target for the treatment of cardiovascular diseases in recent years.<br><br>SEH inhibitors, characterized by their more extensive biological effects such as anti-inflammatory, angiogenesic, antihytrogenic, throovascular, etc., have become a new hot spot in the treatment of metabolic diseases.<br><br>For the first time, our team found that sEH inhibitors improved early osteoporosis.<br><br>Combined with the basis of the previous research, we propose that a high-fat diet can induce high expression of sEH, stimulate bone-breaking cells, accelerate bone transformation and inflammatory response, and reduce bone angiogenesis and inhibit bone formation by regulating hiF1 alpha/VEGF signal transduction path, so inhibiting sEH can be used for osteoporosis treatment.<br><br>In order to confirm the hypothesis, the LDL ligand gene is intended to be applied to knock out mice to establish a model of hyperlipidemia bone injury, and transcriptional histology and bioinfossy are used to clarify the effect of cyclooxid hydrolyzedase on bone injury in hyperlipidemia mice, to evaluate the effect and transformation of sEH inhibitors on the treatment of hyperlipidemia-related osteopathy and to clarify the effects and transformation prospects of sEH-controlled blood vessels.<br><br>This study was carried out to further provide a reliable molecular basis for the pathogenesis of metabolic osteopathy, and to open up a new therapeutic direction to delay the progression of osteoporosis.

Study on the mechanism of sEH regulating bone angiogenesis and bone loss in LDLR - / - mice with hyperlipidemia<br>Soluble epoxide hydrolase (SEH), as a therapeutic target for cardiovascular diseases, has attracted much attention in recent years.<br>With its anti-inflammatory, angiogenic, hypotensive and vasodilative effects, sEH inhibitors have become a new hotspot in the treatment of metabolic diseases.<br>For the first time, our research group found the improvement effect of Sheh inhibitor on early osteoporosis.<br>Based on previous studies, we propose that high-fat diet can induce high expression of sEH, stimulate the activation of osteoclasts, accelerate bone transformation and inflammatory response, and reduce bone angiogenesis and inhibit bone formation by regulating HIF1 α / VEGF signal transduction pathway. Therefore, inhibition of sEH can be used in the treatment of osteoporosis.<br>In order to confirm the hypothesis, LDL receptor gene is proposed to be used to establish a hyperlipidemic bone injury model in mice with LDL receptor gene knockout. Transcriptomics and bioinformatics methods are used to analyze the role and mechanism of sEH in angiogenesis and osteogenesis, to clarify the effect of epoxide hydrolase on bone injury in hyperlipidemic mice, and to evaluate the therapeutic effect of sEH inhibitors on hyperlipidemic bone diseases Objective to elucidate the molecular mechanism of sEH regulating femoral angiogenesis.<br>The purpose of this study is to provide a reliable molecular basis for the pathogenesis of metabolic bone disease, and to open up a new treatment direction for delaying the progress of osteoporosis.