Department of Pharmaceutical Analysis, School of Pharmacy, Ningxia Medical University, 1160 Shenli Street, Yinchuan 750004, China.
School of Clinical Medicine, Ningxia Medical University, 692 Shenli Street, Yinchuan 750004, China.
Oxid Med Cell Longev. 2019 Jun 27;2019:2370862. doi: 10.1155/2019/2370862. eCollection 2019.
The present study was designed to estimate the antiosteoporotic activity of total phenylethanoid glycoside fraction isolated from (CDP) on rats induced by ovariectomy (OVX) as well as the related mechanisms. After 3 months of oral administration, the decreased bone mineral density, serum Ca, and P in OVX rats were recovered and the deteriorated trabecular bone microarchitecture was partly improved by CDP (60, 120, and 240 mg/kg) intervention, the activities of bone resorption markers were downregulated, and the bioactive of the bone formation index was upregulated; meanwhile, the content of MDA was declined, and GSH was increased by CDP treatment. Compositionally, 8 phenylethanoid glycoside compounds were identified in CDP, with the total contents quantified as 50.3% by using the HPLC method. Mechanistically, CDP declined the levels of TRAF6, RANKL, and RANK, thus suppressing RANKL/RANK/TRAF6-induced activation of downstream NF-B and PI3K/AKT signaling pathways and ultimately preventing activities of the key osteoclastogenic proteins of NFAT2 and c-Fos. All of the above data implied that CDP exhibited beneficial effects on bone microstructure in ovariectomized rats, and these effects may be related to the NF-B and PI3K/AKT signaling pathways which were triggered by the binding of RANKL, RANK, and TRAF6.
本研究旨在评估从 （CDP）中分离得到的总苯乙醇苷级分对去卵巢（OVX）大鼠的抗骨质疏松活性及其相关机制。经过 3 个月的口服给药，CDP（60、120 和 240mg/kg）干预可恢复去卵巢大鼠的骨密度、血清 Ca 和 P 降低，改善受损的小梁骨微结构，下调骨吸收标志物的活性，上调骨形成指数的生物活性；同时，CDP 处理可降低 MDA 的含量，增加 GSH 的含量。通过 HPLC 法测定，CDP 中鉴定出 8 种苯乙醇苷化合物，其总含量为 50.3%。从机制上讲，CDP 降低了 TRAF6、RANKL 和 RANK 的水平，从而抑制了 RANKL/RANK/TRAF6 诱导的下游 NF-B 和 PI3K/AKT 信号通路的激活，并最终阻止了 NFAT2 和 c-Fos 等关键破骨细胞生成蛋白的活性。所有上述数据表明，CDP 对去卵巢大鼠的骨微结构具有有益的影响，这些影响可能与 NF-B 和 PI3K/AKT 信号通路有关，该信号通路是由 RANKL、RANK 和 TRAF6 的结合触发的。
