The inhibitory effect and the molecular mechanism of glabridin on RANKL-induced osteoclastogenesis in RAW264.7 cells

2011 ◽  
Author(s):  
Seung Lee
Keyword(s):  
Molecular Mechanism ◽  
Inhibitory Effect ◽  
Raw264.7 Cells

Urea inhibits hypertonicity-inducible TonEBP expression and action

2001 ◽  
Vol 280 (5) ◽  
pp. F904-F912 ◽  
Author(s):  
Wei Tian ◽  
David M. Cohen
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanism ◽  
Reporter Gene ◽  
Gene Transcription ◽  
Phorbol Ester ◽  
Renal Medulla ◽  
Inhibitory Effect ◽  
Characteristic Set ◽  
Enhancer Element ◽  
Enhancer Binding Protein

Tonicity-responsive genes are regulated by the TonE enhancer element and the tonicity-responsive enhancer binding protein (TonEBP) transcription factor with which it interacts. Urea, a permeant solute coexistent with hypertonic NaCl in the mammalian renal medulla, activates a characteristic set of signaling events that may serve to counteract the effects of NaCl in some contexts. Urea inhibited the ability of hypertonic stressors to increase expression of TonEBP mRNA and also inhibited tonicity-inducible TonE-dependent reporter gene activity. The permeant solute glycerol failed to reproduce these effects, as did cell activators including peptide mitogens and phorbol ester. The inhibitory effect of urea was evident as late as 2 h after the application of hypertonicity. Pharmacological inhibitors of known urea-inducible signaling pathways failed to abolish the inhibitory effect of urea. TonEBP action is incompletely understood, but evidence supports a role for proteasome function and p38 action in regulation; urea failed to inhibit proteasome function or p38 signaling in response to hypertonicity. Consistent with its effect on TonEBP expression and action, urea pretreatment inhibited the effect of hypertonicity on expression of the physiological effector gene, aldose reductase. Taken together, these data 1) define a molecular mechanism of urea-mediated inhibition of tonicity-dependent signaling, and 2) underscore a role for TonEBP abundance in regulating TonE-mediated gene transcription.

Sageretia thea Inhibits Inflammation through Suppression of NF-κB and MAPK and Activation of Nrf2/HO-1 Signaling Pathways in RAW264.7 Cells

2019 ◽  
Vol 47 (02) ◽  
pp. 385-403 ◽  
Author(s):  
Ha Na Kim ◽  
Gwang Hun Park ◽  
Su Bin Park ◽  
Jeong Dong Kim ◽  
Hyun Ji Eo ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Mapk Signaling ◽  
Inflammatory Activity ◽  
Nuclear Accumulation ◽  
Raw264.7 Cells ◽  
No Production ◽  
Immunodeficiency Virus ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Signaling Activation

Sageretia thea (S. thea) commonly known as Chinese sweet plum or Chinese bird plum has been used for treating hepatitis and fevers in Korea and China. S. thea has been reported to exert anti-oxidant, anticancer and anti-human immunodeficiency virus activity. However, there is little study on the anti-inflammatory activity of S. thea. Thus, we evaluated the anti-inflammatory effect of extracts of leaves (ST-L) and branches (ST-B) from Sageretia thea in LPS-stimulated RAW264.7 cells. ST-L and ST-B significantly inhibited the production of the pro-inflammatory mediators such as NO, iNOS, COX-2, IL-1[Formula: see text] and IL-6 in LPS-stimulated RAW264.7 cells. ST-L and ST-B blocked LPS-induced degradation of I[Formula: see text]B-[Formula: see text] and nuclear accumulation of p65, which resulted in the inhibition of NF-[Formula: see text]B activation in RAW264.7 cells. ST-L and ST-B also attenuated the phosphorylation of ERK1/2, p38 and JNK in LPS-stimulated RAW264.7 cells. In addition, ST-L and ST-B increased HO-1 expression in RAW264.7 cells, and the inhibition of HO-1 by ZnPP reduced the inhibitory effect of ST-L and ST-B against LPS-induced NO production in RAW264.7 cells. Inhibition of p38 activation and ROS elimination attenuated HO-1 expression by ST-L and ST-B, and ROS elimination inhibited p38 activation induced by ST-L and ST-B. ST-L and ST-B dramatically induced nuclear accumulation of Nrf2, but this was significantly reversed by the inhibition of p38 activation and ROS elimination. Collectively, our results suggest that ST-L and ST-B exerts potential anti-inflammatory activity by suppressing NF-[Formula: see text]B and MAPK signaling activation, and activating HO-1 expression through the nuclear accumulation of Nrf2 via ROS-dependent p38 activation. These findings suggest that ST-L and ST-B may have great potential for the development of anti-inflammatory drug to treat acute and chronic inflammatory disorders.

The molecular mechanism of fullerene-inhibited aggregation of Alzheimer's β-amyloid peptide fragment

Nanoscale ◽  
2014 ◽  
Vol 6 (16) ◽  
pp. 9752-9762 ◽  
Author(s):  
Luogang Xie ◽  
Yin Luo ◽  
Dongdong Lin ◽  
Wenhui Xi ◽  
Xinju Yang ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Inhibitory Effect ◽  
Amyloid Peptide ◽  
Peptide Fragment ◽  
Experiment Study ◽  
Simulation And Experiment ◽  
Β Amyloid ◽  
Combined Simulation ◽  
Β Amyloid Peptide ◽  
Β Sheet

A combined simulation and experiment study demonstrates that fullerenes inhibit the β-sheet formation of Aβ(16–22) and fullerene hexagonal rings play a significant role on the inhibitory effect.

Inhibitory effect of activin A on activation of lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells

Cytokine ◽  
2008 ◽  
Vol 42 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Shi-Yao Wang ◽  
Gui-Xiang Tai ◽  
Peng-Yu Zhang ◽  
Da-Peng Mu ◽  
Xue-Jun Zhang ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Activin A ◽  
Raw264.7 Cells ◽  
Mouse Macrophage
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