摘要
目的研究梅花鹿茸I型胶原(SDC-I)对MC3T3-E1细胞TGF-β1及Smad2/3基因蛋白的影响,探究SDC-I治疗骨质疏松的作用机制。方法分别用不同浓度的SDC-I处理小鼠成骨细胞MC3T3-E1。采用MTT法检测MC3T3-E1细胞增殖活性;应用RT-PCR及ELISA方法检测MC3T3-E1细胞TGF-β1/Smad通路相关因子TGF-β1、Smad2和Smad3的m RNA及蛋白表达水平。结果 SDC-I促进MC3T3-E1细胞的增殖;SDC-I不同浓度作用于MC3T3-E1细胞48 h以后,能显著上调TGF-β1、Smad2以及Smad3基因蛋白表达的水平。与空白对照组相比具有显著性差异,同时SDC-I的浓度越高,效果越明显。结论 SDC-I能刺激MC3T3-E1细胞Smad 2/3和TGF-β1的表达,可通过TGF-β1/Smad信号通路促进骨的形成,为骨质疏松症的防治提供理论依据。
Objective To study the effects of type I collagen(SDC-I) on TGF-β1 and Smad2/3 gene protein in MC3 T3-E1 cells, and to explore the mechanism of SDC-I in the treatment of osteoporosis. Methods MC3 T3-E1 cells were treated with different concentrations of SDC-I. MTT assay was used to detect the proliferation activity of MC3 T3-E1 cells. RT-PCR and ELISA assay were used to detect mRNA and protein expression of TGF-β1, Smad2 and Smad3 of TGF-β1/Smad pathway. Results SDC-I promoted the proliferation of MC3 T3-E1 cells. Different concentrations of SDC-I acted on MC3 T3-E1 cells for 48 h, which could significantly up-regulate the expression of TGF-β1, Smad2, and Smad3 genes and proteins expression. There was a significant difference compared with the blank control group, and the higher the SDC-I concentration, the more signifi cant the effect. Conclusion SDC-I can stimulate the and expression of Smad 2/3 and TGF-β1 in MC3 T3-E1 cells, and promote bone formation through TGF-β1/Smad signal pathway, providing a theoretical basis for the prevention and treatment of osteoporosis.
作者
阚默
石晓征
曲晓波
KAN Mo;SHI Xiaozheng;QU Xiaobo(Changchun University of Chinese Medicine,Changchun 130117,China)
出处
《长春中医药大学学报》
2018年第5期857-860,共4页
Journal of Changchun University of Chinese Medicine
基金
吉林省卫生计生委青年科技骨干培养计划项目(2016Q050)