scholarly journals Genistein suppresses tumor necrosis factor α-induced inflammation via modulating reactive oxygen species/Akt/nuclear factor ΚB and adenosine monophosphate-activated protein kinase signal pathways in human synoviocyte MH7A cells

2014 ◽  
pp. 315 ◽  
Author(s):  
Jinchao Li ◽  
Ruoxi Liu ◽  
Peng Zhang ◽  
Jun Li ◽  
Ye Yue ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis ◽  
Nuclear Factor Kappa B ◽  
Adenosine Monophosphate ◽  
Signal Pathways ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Melatonin Rescued Reactive Oxygen Species-Impaired Osteogenesis of Human Bone Marrow Mesenchymal Stem Cells in the Presence of Tumor Necrosis Factor-Alpha

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xianjian Qiu ◽  
Xudong Wang ◽  
Jincheng Qiu ◽  
Yuanxin Zhu ◽  
Tongzhou Liang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Osteogenic Differentiation ◽  
Tumor Necrosis ◽  
Ros Generation ◽  
Oxygen Species ◽  
Necrosis Factor Alpha ◽  
Marrow Mesenchymal Stem Cells ◽  
Factor Alpha ◽  
Necrosis Factor

Accumulation of reactive oxygen species (ROS), which can be induced by inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), can significantly inhibit the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). This process can contribute to the imbalance of bone remodeling, which ultimately leads to osteoporosis. Therefore, reducing the ROS generation during osteogenesis of BMSCs may be an effective way to reverse the impairment of osteogenesis. Melatonin (MLT) has been reported to act as an antioxidant during cell proliferation and differentiation, but its antioxidant effect and mechanism of action during osteogenesis of MSCs in the inflammatory microenvironment, especially in the presence of TNF-α, remain unknown and need further study. In our study, we demonstrate that melatonin can counteract the generation of ROS and the inhibitory osteogenesis of BMSCs induced by TNF-α, by upregulating the expression of antioxidases and downregulating the expression of oxidases. Meanwhile, MLT can inhibit the phosphorylation of p65 protein and block the degradation of IκBα protein, thus decreasing the activity of the NF-κB pathway. This study confirmed that melatonin can inhibit the generation of ROS during osteogenic differentiation of BMSCs and reverse the inhibition of osteogenic differentiation of BMSCs in vitro, suggesting that melatonin can antagonize TNF-α-induced ROS generation and promote the great effect of osteogenic differentiation of BMSCs. Accordingly, these findings provide more evidence that melatonin can be used as a candidate drug for the treatment of osteoporosis.

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