Bushenhuoxue formula promotes osteogenic differentiation of growth plate chondrocytes through β-catenin-dependent manner during osteoporosis

[Display omitted] Bushenhuoxue formula (BSHXF) has shown excellent clinical effects on the treatment of osteoporosis in China. The aim of this study is to determine the anti-osteoporosis effects and precise molecular mechanisms of BSHXF on mouse models. Ten-week-old female C57BL/6 J mice were subjec...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2020-07, Vol.127, p.110170-110170, Article 110170
Hauptverfasser: Xia, Chenjie, Zou, Zhen, Fang, Liang, Ge, Qinwen, Zhang, Peng, Xu, Huihui, Xu, Rui, Shi, Zhenyu, Lin, Houfu, Ding, Xinyi, Xiao, Luwei, Tong, Peijian, Wang, Ping-er, Jin, Hongting
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container_title Biomedicine & pharmacotherapy
container_volume 127
creator Xia, Chenjie
Zou, Zhen
Fang, Liang
Ge, Qinwen
Zhang, Peng
Xu, Huihui
Xu, Rui
Shi, Zhenyu
Lin, Houfu
Ding, Xinyi
Xiao, Luwei
Tong, Peijian
Wang, Ping-er
Jin, Hongting
description [Display omitted] Bushenhuoxue formula (BSHXF) has shown excellent clinical effects on the treatment of osteoporosis in China. The aim of this study is to determine the anti-osteoporosis effects and precise molecular mechanisms of BSHXF on mouse models. Ten-week-old female C57BL/6 J mice were subjected to ovariectomy and provided a daily treatment of BSHXF. At 8 weeks post-surgery, the femurs were harvested for tissue analyses including μCT, histology, qRT-PCR and immunohistochemical (IHC) staining of β-catenin, ALP and FABP4. To investigate the role of β-catenin in the anti-osteoporosis effects of BSHXF, relative experiments mentioned above were performed in β-catenin conditional knockout mice. Ovariectomized (OVX) mice presented severe bone loss and excessive fat accumulation in the chondro-osseous junction underneath the growth plate, with decreased expression of ALP and increased expression of FABP4. BSHXF significantly recovered the OVX-induced abnormal osteogenesis and adipogenesis with the activation of β-catenin in growth plate chondrocytes. Further, we generated growth plate chondrocyte-specific β-catenin knockout (β-cateninGli1ER) mice that exhibited bone loss and fat accumulation in the chondro-osseous junction, similar to the OVX mice. However, BSHXF failed to rescue the osteoporosis-like phenotype in β-cateninGli1ER mice, indicating the anti-osteoporosis effects of BSHXF act mainly through β-catenin signaling. No significant restoration of ALP and FABP4 was observed in β-cateninGli1ER mice after the treatment of BSHXF. BSHXF attenuates osteoporosis by promoting osteogenic differentiation of growth plate chondrocytes mainly in β-catenin-dependent manner. BSHXF is considered as a new candidate for the treatment of osteoporosis.
doi_str_mv 10.1016/j.biopha.2020.110170
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The aim of this study is to determine the anti-osteoporosis effects and precise molecular mechanisms of BSHXF on mouse models. Ten-week-old female C57BL/6 J mice were subjected to ovariectomy and provided a daily treatment of BSHXF. At 8 weeks post-surgery, the femurs were harvested for tissue analyses including μCT, histology, qRT-PCR and immunohistochemical (IHC) staining of β-catenin, ALP and FABP4. To investigate the role of β-catenin in the anti-osteoporosis effects of BSHXF, relative experiments mentioned above were performed in β-catenin conditional knockout mice. Ovariectomized (OVX) mice presented severe bone loss and excessive fat accumulation in the chondro-osseous junction underneath the growth plate, with decreased expression of ALP and increased expression of FABP4. BSHXF significantly recovered the OVX-induced abnormal osteogenesis and adipogenesis with the activation of β-catenin in growth plate chondrocytes. Further, we generated growth plate chondrocyte-specific β-catenin knockout (β-cateninGli1ER) mice that exhibited bone loss and fat accumulation in the chondro-osseous junction, similar to the OVX mice. However, BSHXF failed to rescue the osteoporosis-like phenotype in β-cateninGli1ER mice, indicating the anti-osteoporosis effects of BSHXF act mainly through β-catenin signaling. No significant restoration of ALP and FABP4 was observed in β-cateninGli1ER mice after the treatment of BSHXF. BSHXF attenuates osteoporosis by promoting osteogenic differentiation of growth plate chondrocytes mainly in β-catenin-dependent manner. 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The aim of this study is to determine the anti-osteoporosis effects and precise molecular mechanisms of BSHXF on mouse models. Ten-week-old female C57BL/6 J mice were subjected to ovariectomy and provided a daily treatment of BSHXF. At 8 weeks post-surgery, the femurs were harvested for tissue analyses including μCT, histology, qRT-PCR and immunohistochemical (IHC) staining of β-catenin, ALP and FABP4. To investigate the role of β-catenin in the anti-osteoporosis effects of BSHXF, relative experiments mentioned above were performed in β-catenin conditional knockout mice. Ovariectomized (OVX) mice presented severe bone loss and excessive fat accumulation in the chondro-osseous junction underneath the growth plate, with decreased expression of ALP and increased expression of FABP4. BSHXF significantly recovered the OVX-induced abnormal osteogenesis and adipogenesis with the activation of β-catenin in growth plate chondrocytes. Further, we generated growth plate chondrocyte-specific β-catenin knockout (β-cateninGli1ER) mice that exhibited bone loss and fat accumulation in the chondro-osseous junction, similar to the OVX mice. However, BSHXF failed to rescue the osteoporosis-like phenotype in β-cateninGli1ER mice, indicating the anti-osteoporosis effects of BSHXF act mainly through β-catenin signaling. No significant restoration of ALP and FABP4 was observed in β-cateninGli1ER mice after the treatment of BSHXF. BSHXF attenuates osteoporosis by promoting osteogenic differentiation of growth plate chondrocytes mainly in β-catenin-dependent manner. 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pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xia, Chenjie</au><au>Zou, Zhen</au><au>Fang, Liang</au><au>Ge, Qinwen</au><au>Zhang, Peng</au><au>Xu, Huihui</au><au>Xu, Rui</au><au>Shi, Zhenyu</au><au>Lin, Houfu</au><au>Ding, Xinyi</au><au>Xiao, Luwei</au><au>Tong, Peijian</au><au>Wang, Ping-er</au><au>Jin, Hongting</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bushenhuoxue formula promotes osteogenic differentiation of growth plate chondrocytes through β-catenin-dependent manner during osteoporosis</atitle><jtitle>Biomedicine &amp; pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2020-07</date><risdate>2020</risdate><volume>127</volume><spage>110170</spage><epage>110170</epage><pages>110170-110170</pages><artnum>110170</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>[Display omitted] Bushenhuoxue formula (BSHXF) has shown excellent clinical effects on the treatment of osteoporosis in China. The aim of this study is to determine the anti-osteoporosis effects and precise molecular mechanisms of BSHXF on mouse models. Ten-week-old female C57BL/6 J mice were subjected to ovariectomy and provided a daily treatment of BSHXF. At 8 weeks post-surgery, the femurs were harvested for tissue analyses including μCT, histology, qRT-PCR and immunohistochemical (IHC) staining of β-catenin, ALP and FABP4. To investigate the role of β-catenin in the anti-osteoporosis effects of BSHXF, relative experiments mentioned above were performed in β-catenin conditional knockout mice. Ovariectomized (OVX) mice presented severe bone loss and excessive fat accumulation in the chondro-osseous junction underneath the growth plate, with decreased expression of ALP and increased expression of FABP4. BSHXF significantly recovered the OVX-induced abnormal osteogenesis and adipogenesis with the activation of β-catenin in growth plate chondrocytes. Further, we generated growth plate chondrocyte-specific β-catenin knockout (β-cateninGli1ER) mice that exhibited bone loss and fat accumulation in the chondro-osseous junction, similar to the OVX mice. However, BSHXF failed to rescue the osteoporosis-like phenotype in β-cateninGli1ER mice, indicating the anti-osteoporosis effects of BSHXF act mainly through β-catenin signaling. No significant restoration of ALP and FABP4 was observed in β-cateninGli1ER mice after the treatment of BSHXF. BSHXF attenuates osteoporosis by promoting osteogenic differentiation of growth plate chondrocytes mainly in β-catenin-dependent manner. BSHXF is considered as a new candidate for the treatment of osteoporosis.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>32334373</pmid><doi>10.1016/j.biopha.2020.110170</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Adipogenesis - drug effects
Animals
beta Catenin - genetics
beta Catenin - metabolism
Bushenhuoxue formula
Cell differentiation
Cell Differentiation - drug effects
Chondrocytes - cytology
Chondrocytes - drug effects
Drugs, Chinese Herbal - pharmacology
Female
Growth Plate - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Osteogenesis - drug effects
Osteoporosis
Osteoporosis - drug therapy
Osteoporosis - pathology
Ovariectomy
Wnt Signaling Pathway - drug effects
β-catenin
title Bushenhuoxue formula promotes osteogenic differentiation of growth plate chondrocytes through β-catenin-dependent manner during osteoporosis
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