软骨组织工程材料尚未涉及金属。前期研究发现镁合金能通过影响TRPM7、p-Akt、CDKs、p21表达，促进软骨细胞增殖。本项目拟在前期研究基础上进一步探讨镁合金促进软骨细胞增殖的分子机制。软骨细胞在含镁合金藻酸盐凝胶中培养，干扰TRPM7基因表达，抑制PI3K/Akt通路，在体外采用分子生物学手段揭示TRPM7、PI3K/Akt通路、p21-CDKs等在镁合金促进软骨细胞增殖中的内在联系；分别影响TRPM7及Akt基因表达，应用PKH26标记软骨细胞后将软骨细胞镁合金藻酸盐凝胶复合体植入兔关节软骨缺损处，采用活体成像技术观察软骨细胞变化，在体内运用分子生物学方法诠释镁合金经TRPM7激活PI3K/Akt通路，调控p21-CDKs表达促进软骨细胞增殖的分子机制，为最终研制出具有优良生物学活性的镁合金软骨组织工程材料奠定基础。

Scaffolds for cartilage tissue engineering has not been made of metal materials. Previous study found that magnesium alloys could promote the proliferation of chondrocyte by regulating the expression of TRPM7, p-Akt, CDKs and p21. Based on previous research, we intend to explore the molecular mechanism of magnesium alloys in promoting the proliferation of chondrocyte. Through the cultivation of chondrocyte in the alginate hydrogel containing magnesium alloys and interfering the expression of TRPM7 and the inhibition of the PI3K/Akt pathway, we want to reveal the intrinsic links between TRPM7, PI3K/Akt signaling pathway, and p21-CDKs in magnesium alloys promoting chondrocyte proliferation in vitro. By interfering the expression of gene TRPM7 and Akt, chondrocyte labeled by PKH26 combined with alginate hydrogel containing magnesium alloys will be implanted into the cartilage defect model of the rabbits. Molecular imaging technique will be used to observe the changes of the chondrocyte; The molecular mechanism of magnesium alloys promoting chondrocyte proliferation through the regulation of p21-CDKs via PI3K/Akt signaling pathway activated by TRPM7 may be revealed using molecular biology methods. Ultimately, this study is expected to lay the foundation for the development of magnesium alloys scaffold of cartilage tissue engineering with excellent biological activity.