Psychosomatic disorders among women with climacteric syndrome during earlier postmenopause

Yelchaninov, D. V.; Аккер, Л. В.; Смагина, И. В.; Gridina, A. O.

doi:10.20538/1682-0363-2009-3(2)-100-103

Cited by 2 publications

(3 citation statements)

References 5 publications

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“…A large number of patients with osteoporosis not only suffer from severe pain, but they are also subjected to a heavy financial burden 2 . In particular, the bone resorption rate of postmenopausal women is significantly higher than that of osteogenesis, leading to a serious bone loss 3 . With the development of ageing population, the number of postmenopausal patients with osteoporosis is increasing year by year, causing a significant impact on the medical community and the whole society 4 .…”

Section: Introductionmentioning

confidence: 99%

“… 2 In particular, the bone resorption rate of postmenopausal women is significantly higher than that of osteogenesis, leading to a serious bone loss. 3 With the development of ageing population, the number of postmenopausal patients with osteoporosis is increasing year by year, causing a significant impact on the medical community and the whole society. 4 At present, the drugs used to treat postmenopausal osteoporosis play a role mainly by inhibiting bone absorption and promoting bone formation.…”

Section: Introductionmentioning

confidence: 99%

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Gentiopicroside promotes the osteogenesis of bone mesenchymal stem cells by modulation of β‐catenin‐BMP2 signalling pathway

Jiang

Zhong

et al. 2021

J Cellular Molecular Medi

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Osteoporosis is characterized by increased bone fragility, and the drugs used at present to treat osteoporosis can cause adverse reactions. Gentiopicroside (GEN), a class of natural compounds with numerous biological activities such as anti‐resorptive properties and protective effects against bone loss. Therefore, the aim of this work was to explore the effect of GEN on bone mesenchymal stem cells (BMSCs) osteogenesis for a potential osteoporosis therapy. In vitro, BMSCs were exposed to GEN at different doses for 2 weeks, whereas in vivo, ovariectomized osteoporosis was established in mice and the therapeutic effect of GEN was evaluated for 3 months. Our results in vitro showed that GEN promoted the activity of alkaline phosphatase, increased the calcified nodules in BMSCs and up‐regulated the osteogenic factors (Runx2, OSX, OCN, OPN and BMP2). In vivo, GEN promoted the expression of Runx2, OCN and BMP2, increased the level of osteogenic parameters, and accelerated the osteogenesis of BMSCs by activating the BMP pathway and Wnt/β‐catenin pathway, effect that was inhibited using the BMP inhibitor Noggin and Wnt/β‐catenin inhibitor DKK1. Silencing the β‐catenin gene and BMP2 gene blocked the osteogenic differentiation induced by GEN in BMSCs. This block was also observed when only β‐catenin was silenced, although the knockout of BMP2 did not affect β‐catenin expression induced by GEN. Therefore, GEN promotes BMSC osteogenesis by regulating β‐catenin‐BMP signalling, providing a novel strategy in the treatment of osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gentiopicroside promotes the osteogenesis of bone mesenchymal stem cells by modulation of β‐catenin‐BMP2 signalling pathway

Jiang

Zhong

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…In particular, the bone resorption rate of postmenopausal women is signi cantly higher than that of osteogenesis, leading to a serious bone loss [3]. With the development of aging population, the number of postmenopausal patients with osteoporosis is increasing year by year, causing a signi cant impact on the medical community and the whole society [4].…”

Section: Introductionmentioning

confidence: 99%

Gentiopicroside promotes osteogenesis and prevents bone loss in ovariectomized mice by modulation of β-catenin-BMP2 signaling pathway

Jiang¹,

Zhong²,

Li³

et al. 2020

Preprint

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Background: Osteoporosis is characterized by increased bone fragility and the drugs used at present to treat osteoporosis can cause adverse reactions. Gentiopicroside (GEN) is widely used in the traditional Chinese medicine thanks to its multiple pharmacological activities including the suppression of osteoclastogenesis. Therefore, the aim of this work was to explore the effect of GEN on bone mesenchymal stem cells (BMSCs) osteogenesis for a potential osteoporosis therapy.Methods: In vitro, BMSCs were exposed to GEN at different doses for 2 weeks, while in vivo, ovariectomized osteoporosis was established in mice and the therapeutic effect of GEN was evaluated for 3 months.Results: Our results in vitro showed that GEN promoted the activity of alkaline phosphatase, increased the calcified nodules in BMSCs and upregulated the osteogenic factors (Runx2, OSX, OCN, OPN, and BMP2). In vivo, GEN strengthened the secretion of Runx2, OCN, and BMP2, increased the level of osteogenic parameters, and accelerated the osteogenesis of BMSCs by activating the BMP pathway and Wnt/β-catenin pathway, effect that was inhibited using the BMP inhibitor Noggin and Wnt/β-catenin inhibitor DKK1. Silencing the β-catenin gene and BMP2 gene blocked the osteogenic differentiation induced by GEN in BMSCs. This block was also observed when only β-catenin was silenced, while the knockout of BMP2 did not affect β-catenin expression induced by GEN. Interpretation.Conclusions: GEN promotes BMSC osteogenesis by regulating β-catenin-BMP signalling, providing a novel strategy in the treatment of osteoporosis.

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Psychosomatic disorders among women with climacteric syndrome during earlier postmenopause

Cited by 2 publications

References 5 publications

Gentiopicroside promotes the osteogenesis of bone mesenchymal stem cells by modulation of β‐catenin‐BMP2 signalling pathway

Gentiopicroside promotes the osteogenesis of bone mesenchymal stem cells by modulation of β‐catenin‐BMP2 signalling pathway

Gentiopicroside promotes osteogenesis and prevents bone loss in ovariectomized mice by modulation of β-catenin-BMP2 signaling pathway

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