<i>Alpinia officinarum</i> Stimulates Osteoblast Mineralization and Inhibits Osteoclast Differentiation

Shim, Ki-Shuk; Lee, Chung-Jo; Yim, Nam–Hui; Gu, Min; Yeul, Jin

doi:10.1142/s0192415x16500701

Cited by 11 publications

(15 citation statements)

References 35 publications

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“…The three-point bending test was utilized to determine the bone biomechanical properties. Based on the test results, microstructural parameters [ 42 ], such as BV/TV, Tb.Th, Tb.N, Tb.Sp, Conn.D, SMI, and BMD improved with use of GSTD compared to long-term large-dose DEX treatment. Moreover, ultimate breaking force and bone stiffness increased, reflecting the enhancement by GSTD compared to the control and DEX.…”

Section: Discussionmentioning

confidence: 99%

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Gastrodin alleviates glucocorticoid induced osteoporosis in rats via activating the Nrf2 signaling pathways

et al. 2018

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BackgroundProlonged and over-dosed administration of glucocorticoids results in more bone remodeling, leading to glucocorticoid-induced osteoporosis, which is primarily due to dysfunction and apoptosis of osteoblasts. The present study investigated the therapeutic effect and molecular mechanism of gastrodin, a natural bioactive compound isolated from the traditional Chinese herbal agent Gastrodia elata, on osteoblastic cells in vivo and in vitro.Materials and MethodsThe anti-dexamethasone (DEX) effects of gastrodin on primary osteoblasts were measured by cell viability, flow cytometry, and western blot analysis in vitro, and also extensively examined in a rat model in vivo.ResultsThe results show that gastrodin pretreatment significantly increased osteoblast viability and alkaline phosphatase activity when exposed to DEX. Alizarin Red staining indicated more calcium deposits formed in the gastrodin pretreatment against DEX group. Gastrodin alleviated DEX-induced reactive oxygen species at both the mitochondrial and cellular levels in osteoblasts. In addition, gastrodin protected primary osteoblasts from caspase3-related apoptosis by reducing the loss in the mitochondrial membrane potential and decreasing the release of DEX-induced cytochrome-C, bax, and apoptosis inducing factor. Gastrodin also antagonized upregulated endoplasmic reticulum stress signals induced by DEX, including the expression of GRP78, CHOP, and phosphorylated eIF2α. Furthermore, gastrodin protected osteoblasts by activating the nuclear factor erythroid derived 2-related factor-2 (Nrf2) pathway. Furthermore, femoral micro-computed tomography scans and biomechanical tests revealed that gastrodin improved bone microstructure and mitigated DEX-induced deterioration in bone quality.ConclusionsThese findings suggest that gastrodin alleviated glucocorticoid-induced osteoporosis in rats by protecting osteoblasts via the Nrf2 regulated mitochondrial and ER stress-related signaling pathways.

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Section: Discussionmentioning

confidence: 99%

“…Primary osteoblasts were isolated from neonatal rats as described previously [ 42 ]. The calvaria were removed from the rats and moderately digested with 0.25% trypsin at 37°C for 30 min.…”

Section: Methodsmentioning

confidence: 99%

Gastrodin alleviates glucocorticoid induced osteoporosis in rats via activating the Nrf2 signaling pathways

et al. 2018

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“…Primary osteoblasts were isolated from neonatal rats as described previously ( Shim et al, 2016 ). Cells were resuspended and maintained in DMEM high glucose supplemented with 20% fetal bovine serum (FBS; PAN-Biotech, Adenbach, Germany), 100 U/mL penicillin, and 100 μg/mL streptomycin, in a 5% CO 2 humidified atmosphere at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Epigallocatechin-3-Gallate Ameliorates Glucocorticoid-Induced Osteoporosis of Rats in Vivo and in Vitro

Liu

Yang

et al. 2018

Front. Pharmacol.

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Background: Prolonged administration of overdoses of glucocorticoids results in increased bone remodeling, leading to glucocorticoid-induced osteoporosis (GIO), which is primarily due to the dysfunction and apoptosis of osteoblasts. The present study investigated the therapeutic effect and molecular mechanism of action of epigallocatechin-3-gallate (EGCG), a bioactive catechin in green tea, in high-dose dexamethasone-induced osteoblast differentiation in vivo and in vitro.Methods: The anti-dexamethasone (DEX) effects of EGCG on primary osteoblasts were determined on the basis of cell viability and alkaline phosphatase (ALP) and total cellular superoxide dismutase (SOD) activities. Flow cytometry and Western blot analysis were also used to evaluate the expression of related biomarkers in vitro, and bone microarchitecture was also extensively examined in a rat model in vivo.Results: The results showed that EGCG pretreatment significantly increased osteoblast viability and ALP and SOD activities when cells were exposed to DEX. Alizarin red staining indicated that there was more mineralization with EGCG pretreatment, countering DEX effects. EGCG reduced DEX-induced reactive oxygen species at both the mitochondrial and cellular levels in osteoblasts by activating the nuclear factor erythroid-derived 2-like-2 (Nrf2) pathway. In addition, EGCG protected osteoblasts from apoptosis. EGCG also regulated the formation of active glucocorticoid by 11β-hydroxysteroid dehydrogenase activity. Furthermore, femoral micro-computed tomography scans revealed that EGCG improved bone microstructure and mitigated DEX-induced deterioration of bone quality.Conclusion: These findings suggested that EGCG reversed GIO in rats by protecting osteoblasts by activating the Nrf2 signaling pathway.

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“…These flavonoids have been reported to enhance osteoblastic differentiation and activity. 21,32,33 According to our results, the flavonoids did not have high toxicity, and the survival rates of 5 µM treatment of galangin and kaempferol increased time dependently ( Figure 3A). The cytoprotective effects of flavonoids were confirmed using an MTT assay and Western blot analysis.…”

Section: Flavonoids Show Cytoprotective Effects Against Zoledronatementioning

confidence: 58%

Cytoprotective effect of flavonoid‐induced autophagy on bisphosphonate mediated cell death in osteoblast

Kim

et al. 2018

J of Cellular Biochemistry

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With rapid economic growth and further developments in medical science, the entry into the aging population is currently increasing, as is the number of patients with metabolic diseases, such as hypertension, hyperlipidemia, heart disease, and diabetes. The current treatments for metabolic bone diseases, which are also on the rise, cause negative side effects. Bisphosphonates, which are used to treat osteoporosis, inhibit the bone resorption ability of osteoclasts and during prolonged administration, cause bisphosphonate‐related osteonecrosis of the jaw (BRONJ). Numerous studies have shown the potential role of natural plant products as flavonoids in the protection against osteoporosis and in the influence of bone remodeling. Autophagy occurs after the degradation of cytoplasmic components within the lysosome and serves as an essential cytoprotective response to pathologic stress caused by certain diseases. In the present study, we hypothesized that the cytoprotective effects of flavonoids might be related to those associated with autophagy, an essential cytoprotective response to the pathologic stress caused by certain diseases, in osteoblasts. We demonstrated the cytoprotective effect of flavonoid‐induced autophagy against the toxicity of zoledronate and the induction of autophagy by flavonoids to support osteogenic transcription factors, leading to osteoblast differentiation and bone formation. Further studies are necessary to clarify the connections between autophagy and osteogenesis. It would be helpful to shed light on methodological challenges through molecular biological studies and new animal models. The findings of the current study may help to delineate the potential role of flavonoids in the treatment of metabolic bone disease.

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Alpinia officinarum Stimulates Osteoblast Mineralization and Inhibits Osteoclast Differentiation

Cited by 11 publications

References 35 publications

Gastrodin alleviates glucocorticoid induced osteoporosis in rats via activating the Nrf2 signaling pathways

Gastrodin alleviates glucocorticoid induced osteoporosis in rats via activating the Nrf2 signaling pathways

Epigallocatechin-3-Gallate Ameliorates Glucocorticoid-Induced Osteoporosis of Rats in Vivo and in Vitro

Cytoprotective effect of flavonoid‐induced autophagy on bisphosphonate mediated cell death in osteoblast

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