Abstract
Yishen Bugu Ye (YSBGY), a traditional Chinese medicine comprising 12 types of medicinal herbs, is often prescribed in China to increase bone strength. In this study, the antiosteoporotic effects of YSBGY were investigated in C57BL/6 mice afflicted with dexamethasone- (Dex-) induced osteoporosis (OP). The results showed that YSBGY reduced the interstitial edema in the liver and kidney of mice with Dex-induced OP. It also increased the number of trabecular bone elements and chondrocytes in the femur, promoted cortical bone thickness and trabecular bone density, and modulated the OP-related indexes in the femur and tibia of OP mice. It also increased the serum concentrations of type I collagen, osteocalcin, osteopontin, bone morphogenetic protein-2, bone morphogenetic protein receptor type 2, C-terminal telopeptide of type I collagen, and runt-related transcription factor-2 and reduced those of tartrate-resistant acid phosphatase 5 and nuclear factor of activated T cells in these mice, suggesting that it improved osteoblast differentiation and suppressed osteoclast differentiation. The anti-inflammatory effect of YSBGY was confirmed by the increase in the serum concentrations of interleukin- (IL-) 33 and the decrease in concentrations of IL-1, IL-7, and tumor necrosis factor-α in OP mice. Furthermore, YSBGY enhanced the serum concentrations of superoxide dismutase and catalase in these mice, indicating that it also exerted antioxidative effects. This is the first study to confirm the antiosteoporotic effects of YSBGY in mice with Dex-induced OP, and it showed that these effects may be related to the YSBGY-induced modulation of the osteoblast/osteoclast balance and serum concentrations of inflammatory factors. These results provide experimental evidence supporting the use of YSBGY for supporting bone formation in the clinical setting.
Highlights
Osteoporosis (OP) is a metabolic skeletal disorder characterized by decreased bone mass and microstructural destruction of bone tissue [1] and can be divided into primary and secondary OP [2]
Low body weights were observed in mice with Dex-induced OP (P < 0:001, Table 1), which were not reversed after Yishen Bugu Ye (YSBGY) or E2 administration (Table 1)
We found that seven-week YSBGY administration resulted in a 22.0%, 13.6%, 26.5%, 12.9%, 20.2%, and 43.2% decrease in the serum concentrations of COL-I, bone gla protein (BGP), OCN, OPN, bone morphogenetic protein2 (BMP-2), bone morphogenetic protein receptor type 2 (BMPR-2), and CTX-1 and a 16.5% increase in those of TRACP-5β (P < 0:05, Table 2)
Summary
Osteoporosis (OP) is a metabolic skeletal disorder characterized by decreased bone mass and microstructural destruction of bone tissue [1] and can be divided into primary and secondary OP [2]. Together with the increasingly aging population of China, this means that approximately 100 million people are estimated to have low bone mass or OP [5]. Osteoblasts and osteoclasts work synergistically to maintain bone homeostasis. Increase in osteoclast-mediated bone resorption and decrease in osteoblast-mediated bone formation disrupt the osteoclast/osteoblast balance, leading to OP [6, 7]. During the bone formation process, osteoblasts form new bone directly through the synthesis and secretion of bone-associated proteins and indirectly control osteoclast-mediated bone resorption [7]. Oxidative stress regulates bone homeostasis, and a redox imbalance can promote osteoblast apoptosis and induce osteoclast differentiation, contributing to the osteoclast/osteoblast imbalance and leading to OP [8]. The commonly used therapeutic agents for OP, such as denosumab and vitamin D, reduce bone resorption and exert various adverse
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