Regulation of vitamin D receptor and Genistein on bone metabolism in mouse osteoblasts and the molecular mechanism of osteoporosis.

The aim of this work was to study the mechanisms of vitamin D receptor (VDR) and Genistein (Gen) on the regulation of bone metabolism of phytoestrogens from cellular and epidemiological perspectives. MC3T3-E1 cells were treated with different concentrations of Gen, and the cell-proliferation rate was detected by an MTT colorimetric assay. The effect of the VDR receptor blocker ZK159222 on the Gen effect was then observed; after adding Gen to MC3T3-E1 cells, we detected the expression of VDR protein via Western blotting. After adding estrogen receptor α-blocker MPP and estrogen receptor β-blocker PHTPP, we observed the effect of Gen on the regulation of the VDR protein. DNA was extracted from the blood samples of 200 postmenopausal women in the early epidemiological survey, and the restriction fragment length polymorphism of VDR gene Apa I and Bsm I in each sample was observed. The results were analyzed using dietary survey and bone mineral density examination. The results show that 10-8mol/L Gen can promote the proliferation of MC3T3-E1 cells (P less than 0.05). This effect can be canceled by the VDR blocker ZK159222. By analyzing the Apa I and Bsm I genotypes of VDR restriction sites, we discovered no significant difference in bone mineral density (BMD) between different genotypes (P>0.05). In addition, there was no significant correlation between dietary phytoestrogen intake and BMD in different genotypes (P>0.05). In conclusion, VDR can mediate the effect of Gen on the proliferation of MC3T3-E1 cells. The up-regulated expression of VDR protein in Gen is not mediated by the estrogen receptor. Moreover, the VDR gene polymorphism is not related to the BMD in various parts and is not related to the bone metabolism effect of the dietary plant estrogen intake.