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Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: It is an effective strategy for the treatment of osteoporosis to promote the proliferation and differentiation of osteoblasts, but the influence of inokosterone onosteoblast proliferation and differentiation is rarely reported.OBJECTIVE: To investigate the effects of inokosterone on theproliferation and differentiation of primary osteoblasts and the underlying molecular mechanism.METHODS:Primary osteoblasts from neonatal Sprague-Dawley rats were isolated via the second enzyme digestion, and the cells were then cultured in osteogenic induction medium and identified. Cell counting kit 8 assay was performed to evaluate the effect of different concentrations of inokosterone (1, 5, 10 mg/L) on cell viability of primary osteoblasts. Early differentiation ability of osteoblasts was evaluated by alkaline phosphatase staining and alkaline phosphatase activity assay. To evaluate the mineralization ability of osteoblasts, alizarin red staining was performed to observe the number of calcium nodules. The expression level of osteogenic genes was detected by RT-qPCR at different time points. Furthermore, MDC staining was also used to observe the number of autophagosomes. RESULTS AND CONCLUSION: Compared with the control group, inokosterone could inhibit the cell viability of primary osteoblast to some degree (P < 0.05) while significantly promoting alkaline phosphatase activity and mineralized nodules formation (P< 0.05). In addition, inokosterone upregulated the expression of osteogenic genessuch as Collagen I, osteoprotegerin, osteopontin, osteocalcin and increased the number of autophagosomes. To conclude, inokosterone can promote osteogenic differentiation by upregulating osteogenic genes expression and activating autophagy of primary osteoblasts. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In recent years, molecular signaling pathways related to bone metabolism has become a hot topic. Studies have revealed that signaling pathways associated with osteoporosis include Wnt/β-catenin, RANKL/RANK/OPG, NF-κB, PPAR-γ, PTH, MAPK, PI3K/Akt, Hedgehog and Notch signaling pathways. However, there has been no study concentrated on ERα-AMPK-Sirt1 signaling pathway. Estrogen receptor alpha (ERα), AMP-activated protein kinase (AMPK) and Sirtuin 1(Sirt1) can regulate the function of osteoblast or osteoclast by ligand binding, phosphorylation and deacetylation, respectively. Studies have indicated that ERα can directly increase the activity of LKB1, while LKB1 is the most important upstream protein kinase of AMPK, as a result, AMPK is activated. In addition, the mutual promotion of AMPK and Sirt1 can also modulate the autophagy or apoptosis of osteoblast; all these suggested that ERα-AMPK-Sirt1 signaling pathway may play an important role in the pathogenesis of osteoporosis. To sum up, it is necessary to start the research of ERα-AMPK-Sirt1 signaling pathway in order to better guide the development of new drugs and clinical practice. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)