Int J Nanomed:ERK1/2通路在辛伐他汀负载纳米胶束和辛伐他汀调节MG63细胞成骨作用中的作用

2018-12-29 MedSci MedSci原创

本研究旨在探究ERK1/2通路在负载辛伐他汀(SV)的纳米胶束(SVNs)和SV介导的促进细胞的成骨分化过程中的作用,并探究SVNs在促进成骨分化方面比SV具有更大功效的分子机制。使用透析方法合成SVNs。使用2.5,0.25和0.025μmol/L的药物处理MG63细胞。通过检查MG63细胞的增殖活性和ALP活性来确定最佳药物剂量。随后,使用Western印迹分析以分析每个实验组中在不同时间点的

本研究旨在探究ERK1/2通路在负载辛伐他汀(SV)的纳米胶束(SVNs)和SV介导的促进细胞的成骨分化过程中的作用,并探究SVNs在促进成骨分化方面比SV具有更大功效的分子机制。

使用透析方法合成SVNs。使用2.5,0.25和0.025μmol/L的药物处理MG63细胞。通过检查MG63细胞的增殖活性和ALP活性来确定最佳药物剂量。随后,使用Western印迹分析以分析每个实验组中在不同时间点的磷酸化ERK1/2蛋白的水平。最后,使用抑制剂PD98059抑制ERK1/2通路。分析了MG63细胞和成骨相关标志物的增殖活性的变化。

结果显示,本研究合成的SVNs的平均直径为27nm。包封率和载药效率分别为52.03%±4.05%和9.42%±0.66%。当药物以0.25μmol/L的浓度给药时,SVNs和SV表现出最佳的促骨生成作用。药物诱导的ERK1/2通路激活在给药后15分钟达到峰值,然后迅速下降。从24小时到7天,SVN和SV对ERK1/2通路发挥抑制作用而不是激活作用。在整个实验过程中,SVNs对ERK1/2通路的调节作用明显大于SV。PD98059对ERK1/2通路的抑制显著降低了所有实验组中细胞的增殖活性。此外,ALP活性和osterix(OSX)和骨钙蛋白(OC)蛋白的表达水平明显增加。

综上所述,该研究结果表明,SVN通过强抑制ERK1/2通路显著增加SV诱导的成骨分化的作用。

原始出处:

Niu M, Feng X, Zhou L. The role of the ERK1/2 pathway in simvastatin-loaded nanomicelles and simvastatin in regulating the osteogenic effect in MG63 cells. Int J Nanomedicine. 2018 Dec 5;13:8165-8178. doi: 10.2147/IJN.S182998. eCollection 2018.

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    2019-03-31 chenlianhui
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    2018-12-30 zhaojie88
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