Effect of gomisin A on osteoblast differentiation in high glucose-mediated oxidative stress

Takanche, Jyoti Shrestha; Kim, Jieun; Han, Sung-Hyun; Yi, Ho-Keun

doi:10.1016/j.phymed.2019.153107

Cited by 33 publications

(32 citation statements)

References 34 publications

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“…Osteoclastic bone resorption and osteoblastic bone formation maintain bone homeostasis together, so some experiments on osteoblast were performed as a supplement. In the current study, we found Schisandrin B can promote osteoclast differentiation ( Supplementary Figure 1 ), and these results were partially in agreement with previous studies ( Caichompoo et al, 2009 ; Takanche et al, 2020 ). Osteoblasts are derived from mesenchymal stem cells, and besides osteoblasts, mesenchymal stem cells can also differentiate into other cell types, including adipocytes, myocytes, and chondrocytes ( Jackson et al, 2012 ).…”

Section: Discussionsupporting

confidence: 94%

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

et al. 2020

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Osteoporosis is a systemic skeletal disease which is highly prevalent worldwide and considered to be associated with excessive bone resorption mediated by osteoclast. Osteoclast differentiation is featured by the activation of inflammation-related pathways and the generation of reactive oxygen species. Schisandrin B is a bioactive compound with strong antiinflammation and antioxidative properties, we thus speculated that Schisandrin B might serve as a potential candidate for osteoporosis. In the present study, we found that the formation and` function of osteoclasts were dramatically suppressed by Schisandrin B. And consistent with the in vitro results, treatment with Schisandrin B attenuated ovariectomy-induced bone loss in mice. Moreover, Schisandrin B notably inhibited the activation of mitogen activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways and scavenged ROS by activating nuclear factor E2 p45-related factor 2 (Nrf2) signaling. In conclusion, our study indicates that Schisandrin B is an effective approach to treat osteoporosis and other osteoclast-related diseases.

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Section: Discussionsupporting

confidence: 94%

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

et al. 2020

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“…Long-term exposure to high glucose levels leads to metabolic disturbance, causes oxidative stress and induces ROS accumulation ( 16 ). A previous study reported that glucose oxidative stress induced by high glucose levels interferes with osteoblast differentiation and mineralization ( 27 ). One of the main causes of cell damage is accumulated ROS induced by high glucose levels ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

“…A previous study reported that glucose oxidative stress induced by high glucose levels interferes with osteoblast differentiation and mineralization ( 27 ). One of the main causes of cell damage is accumulated ROS induced by high glucose levels ( 27 ). Mitochondrial biogenesis enhances cellular function, survival and recovery from oxidative-induced cell damage ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondrial biogenesis enhances cellular function, survival and recovery from oxidative-induced cell damage ( 28 ). Targeting glucose-induced ROS and protecting mitochondrial DNA from oxidative stress is considered a promising therapeutic strategy for high glucose-induced inhibition of cell proliferation and osteoblastic differentiation ( 27 ). Takanche et al reported that gomisin A, a lignan isolated from the hexane of Schisandra chinensis fruit extract, protects osteoblast from high glucose-induced oxidative stress and promotes mitochondrial function ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

“…Targeting glucose-induced ROS and protecting mitochondrial DNA from oxidative stress is considered a promising therapeutic strategy for high glucose-induced inhibition of cell proliferation and osteoblastic differentiation ( 27 ). Takanche et al reported that gomisin A, a lignan isolated from the hexane of Schisandra chinensis fruit extract, protects osteoblast from high glucose-induced oxidative stress and promotes mitochondrial function ( 27 ). The results of the present study confirmed that high glucose levels induced ROS accumulation, decreased MMP and caused mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

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Metformin promotes cell proliferation and osteogenesis under high glucose condition by regulating the ROS‑AKT‑mTOR axis

Zhou

Qiu

et al. 2020

Mol Med Rep

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Metformin, a cost-effective and safe orally administered antidiabetic drug used by millions of patients, has exhibited great interest for its potential osteogenic-promoting properties in different types of cells, including mesenchymal stem cells (MSCs). Diabetic osteopathy is a common comorbidity of diabetes mellitus; however, the underlying molecular mechanisms of metformin on the physiological processes of MSCs, under high glucose condition, remain unknown. To determine the effects of metformin on the regulatory roles of proliferation and differentiation in MSCs, under high glucose conditions, osteogenesis after metformin treatment was detected with Alizarin Red S and ALP staining. The results demonstrated that high glucose levels significantly inhibited cell proliferation and osteogenic differentiation under high glucose conditions. Notably, addition of metformin reversed the inhibitory effects induced by high glucose levels on cell proliferation and osteogenesis. Furthermore, high glucose levels significantly decreased mitochondrial membrane potential (MMP), whereas treatment with metformin helped maintain MMP. Further analysis of mitochondrial function revealed that metformin significantly promoted ATP synthesis, mitochondrial DNA mass and mitochondrial transcriptional activity, which were inhibited by high glucose culture. Furthermore, metformin significantly scavenged reactive oxygen species (ROS) induced by high glucose levels, and regulated the ROS-AKT-mTOR axis inhibited by high glucose levels, suggesting the protective effects of metformin against high glucose levels via regulation of the ROS-AKT-mTOR axis. Taken together, the results of the present study demonstrated the protective role of metformin on the physiological processes of MSCs, under high glucose condition and highlighted the potential molecular mechanism underlying the effect of metformin in promoting cell proliferation and osteogenesis under high glucose condition.

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Neobavaisoflavone protects osteoblasts from dexamethasone‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway

Zhu

Wang

et al. 2021

Drug Development Research

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Neobavaisoflavone (NBIF) is a flavonoid, which has a variety of pharmacological activities. However, the mechanism of NBIF in the treatment of osteoporosis still needs further exploration. The differentiation of osteoblast MC‐3T3‐E1 cells after treatment was observed by Alizarin red staining. Cell counting kit‐8 and flow cytometry were used to detect viability, apoptosis, and reactive oxygen species (ROS) levels of treated MC‐3T3‐E1 cells, respectively. Malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) were tested by ELISA kits. The expressions of lncRNA MALAT1, MEG3, CRNDE, Runx2, osteocalcin (OCN), osteopontin (OPN), collagen I (col‐I), nuclear Nrf2, cytoplasm Nrf2, heme oxygenase‐1 (HO‐1) and quinone oxidoreductase 1 (NQO1) in treated MC‐3T3‐E1 cells were examined by Quantitative real‐time PCR or Western blot. Dexamethasone (Dex) inhibited the viability of MC‐3T3‐E1 cells, while the appropriate amount of NBIF had no significantly effect on cell viability. Dex downregulated CRNDE expression, whereas NBIF upregulated CRNDE. Overexpressed CRNDE and NBIF reversed the inhibitory effects of Dex on cell viability, differentiation and levels of SOD, GSH‐Px, Runx2, OCN, OPN, col‐I, nuclear Nrf2, HO‐1 and NQO1 while reversing the promoting effect of Dex on apoptosis and the levels of ROS, MDA, LDH and cytoplasm Nrf2 in MC‐3T3‐E1 cells, respectively, but shCRNDE further reversed the effects of NBIF in MC‐3T3‐E1 cells. NBIF protected osteoblasts from Dex‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway.

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Effect of gomisin A on osteoblast differentiation in high glucose-mediated oxidative stress

Cited by 33 publications

References 34 publications

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

Metformin promotes cell proliferation and osteogenesis under high glucose condition by regulating the ROS‑AKT‑mTOR axis

Neobavaisoflavone protects osteoblasts from dexamethasone‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway

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