Liu Xinhong, Zheng Jiazhuang, Li Fang, Yi Ruokun, Mu Jianfei, Tan Fang, Zhao Xin
Chongqing Collaborative Innovation Center for Functional Food, Chongqing University of Education, Chongqing 400067, China.
Chongqing Engineering Research Center of Functional Food, Chongqing University of Education, Chongqing 400067, China.
Evid Based Complement Alternat Med. 2020 Sep 22;2020:2054389. doi: 10.1155/2020/2054389. eCollection 2020.
A rat model of secondary osteoporosis was constructed using retinoic acid as an inducer, and the genes, proteins, and bone mass of the rats were analyzed. qPCR detection of the Wnt/-catenin and OPG/RANK/RANKL signaling pathway-related gene expression levels showed that HFY15 played a positive role in regulating both pathways. HFY15 significantly increased -catenin, Lrp5, Lrp6, Wnt10b, OPG, RANKL, and Runx2 expression and downregulated DKK1, RANK, CTSK, TRACP, and ALP expression. Enzyme-linked immunosorbent assays further confirmed the qPCR results. Tartrate-resistant acid phosphatase staining showed that HFY15 slowed retinoic acid-induced osteoclast formation. Microcomputed tomography showed that HFY15 reduced trabecular separation and increased the percent bone volume, trabecular numbers, trabecular thickness, and bone mineral density in the rats in vivo. These findings indicate that HFY15 may help prevent retinoic acid-induced secondary osteoporosis in vivo.
以维甲酸为诱导剂构建大鼠继发性骨质疏松模型,并对大鼠的基因、蛋白质和骨量进行分析。qPCR检测Wnt/β-连环蛋白和OPG/RANK/RANKL信号通路相关基因表达水平,结果显示HFY15在调节这两条通路中均发挥正向作用。HFY15显著增加β-连环蛋白、Lrp5、Lrp6、Wnt10b、OPG、RANKL和Runx2的表达,并下调DKK1、RANK、CTSK、TRACP和ALP的表达。酶联免疫吸附测定进一步证实了qPCR结果。抗酒石酸酸性磷酸酶染色显示HFY15减缓了维甲酸诱导的破骨细胞形成。微型计算机断层扫描显示,HFY15减少了体内大鼠的小梁间距,并增加了骨体积百分比、小梁数量、小梁厚度和骨矿物质密度。这些发现表明,HFY15可能有助于预防体内维甲酸诱导的继发性骨质疏松。