Background

Kaempferol has improved the functions of various human diseases. Here, we aimed to probe into the potential molecular mechanism of Kaempferol to ameliorate osteoporosis.

Methods

Micro-computed tomography scanning was applied to assess the bone density of osteoporosis rats induced by ovariectomized. Quantitative real-time PCR was applied to detect the expressions of RUNX2, Osterix, CXCL12, and miR-10a-3p. Western blot, Alizarin red staining, Alkaline Phosphatase Diethanolamine Activity Kit were applied to confirm the in vitro functions of Kaempferol. RNA Immunoprecipitation and dual-luciferase reporter gene experiments were applied to study the potential mechanism.

Results

The treatment of Kaempferol raised bone density in osteoporosis rats induced by ovariectomized, and boosted the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), and raised the expressions of RUNX2, Osterix, and CXCL12, and lessened miR-10a-3p. From the potential mechanism analysis, we corroborated that miR-10a-3p and CXCL12 bound to each other, and Kaempferol boosted BMSC osteogenic differentiation and ameliorated osteoporosis by lessening miR-10a-3p and raising CXCL12.

Conclusion

Our data expounded that Kaempferol boosted BMSC osteogenic differentiation and ameliorated osteoporosis by lessening miR-10a-3p and raising CXCL12.

中文翻译：

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山奈酚通过下调 miR-10a-3p 和上调 CXCL12 促进 BMSC 成骨分化并改善骨质疏松

 背景

山奈酚具有改善人类多种疾病的功能。在这里，我们的目的是探讨山奈酚改善骨质疏松症的潜在分子机制。

 方法

采用显微计算机断层扫描技术评估去势大鼠骨质疏松的骨密度。采用实时定量PCR检测RUNX2、Osterix、CXCL12和miR-10a-3p的表达。采用Western blot、茜素红染色、碱性磷酸酶二乙醇胺活性试剂盒验证山奈酚的体外功能。应用RNA免疫沉淀和双荧光素酶报告基因实验来研究其潜在机制。

 结果

山奈酚治疗可提高去卵巢所致骨质疏松大鼠的骨密度，促进骨髓间充质干细胞（BMSCs）的成骨分化，并上调RUNX2、Osterix和CXCL12的表达，并减少miR-10a-3p的表达。从潜在机制分析中，我们证实了miR-10a-3p和CXCL12相互结合，山奈酚通过减少miR-10a-3p和升高CXCL12来促进BMSC成骨分化并改善骨质疏松。

 结论

我们的数据表明，山奈酚通过减少 miR-10a-3p 和升高 CXCL12 来促进 BMSC 成骨分化并改善骨质疏松症。