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Myricitrin promotes osteogenesis and prevents ovariectomy bone mass loss via the PI3K/AKT signalling pathway

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机构： [1]First School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China. [2]The Laboratory of Orthopaedics and Traumatology of Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, China. [3]Guangzhou First People's Hospital, Second Affiliated Hospital of South China University of Technology, Guangzhou, China. [4]Eighth Clinical School of Guangzhou University of Chinese Medicine, Foshan Hospital of Traditional Chinese Medicine, Foshan, China. [5]Department of Orthopedics, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, China. [6]Department of Orthopaedic Surgery, Wendeng Orthopedic and Traumatologic Hospital of Shandong Province, Weihai, China. [7]Fifth Clinical School of Guangzhou University of Chinese Medicine, Guangdong Second Tradmonal Chinese Medicine Hostpital, Guangzhou, China. [8]Second School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China. [9]Department of Orthopaedic Surgery, Guangzhou Hospital of Integrated Traditional and West Medicine, Guangzhou, China. [10]Department of Orthopaedic Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

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This study aimed to explore the effect of myricitrin on osteoblast differentiation in mice immortalised bone marrow mesenchymal stem cells (imBMSCs). Additionally, ovariectomy (OVX) mice were employed to examine the effect of myricitrin on bone trabecular loss in vivo. The effect of myricitrin on the proliferation of imBMSCs was evaluated using a cell counting kit-8 assay. Alizarin red staining, alkaline phosphatase staining were performed to elucidate osteogenesis. Furthermore, qRT-PCR and western blot determined the expression of osteo-specific genes and proteins. To screen for candidate targets, mRNA transcriptome genes were sequenced using bioinformatics analyses. Western blot and molecular docking analysis were used to examine target signalling markers. Moreover, rescue experiments were used to confirm the effect of myricitrin on the osteogenic differentiation of imBMSCs. OVX mice were also used to estimate the delay capability of myricitrin on bone trabecular loss in vivo using western blot, micro-CT, tartaric acid phosphatase (Trap) staining, haematoxylin and eosin staining, Masson staining and immunochemistry. In vitro, myricitrin significantly enhanced osteo-specific genes and protein expression and calcium deposition. Moreover, mRNA transcriptome gene sequencing and molecular docking analysis revealed that this enhancement was accompanied by an upregulation of the PI3K/AKT signalling pathway. Furthermore, copanlisib, a PI3K inhibitor, partially reversed the osteogenesis promotion induced by myricitrin. In vivo, western blot, micro-CT, hematoxylin and eosin staining, Masson staining, Trap staining and immunochemistry revealed that bone trabecular loss rate was significantly alleviated in the myricitrin low- and high-dose groups, with an increased expression of osteopontin, osteoprotegerin, p-PI3K and p-AKT compared to the OVX group. Myricitrin enhances imBMSC osteoblast differentiation and attenuate bone mass loss partly through the upregulation of the PI3K/AKT signalling pathway. Thus, myricitrin has therapeutic potential as an antiosteoporosis drug.© 2023 Wiley Periodicals LLC.

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出版当年[2022]版：

大类 | 2 区生物学

小类 | 3 区生化与分子生物学 3 区细胞生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 4 区生化与分子生物学 4 区细胞生物学

JCR分区：

出版当年[2021]版：

Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 CELL BIOLOGY

最新[2023]版：

Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 CELL BIOLOGY

影响因子： 3 最新[2023版] 3.1 最新五年平均 4.481 出版当年[2021版] 4.564 出版当年五年平均 4.429 出版前一年[2020版] 4 出版后一年[2022版]

第一作者：

第一作者机构： [1]First School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China. [2]The Laboratory of Orthopaedics and Traumatology of Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, China. [3]Guangzhou First People's Hospital, Second Affiliated Hospital of South China University of Technology, Guangzhou, China.

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通讯作者：

通讯机构： [1]First School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China. [2]The Laboratory of Orthopaedics and Traumatology of Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, China. [10]Department of Orthopaedic Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

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