scholarly journals Vitamin E and telmisartan attenuates doxorubicin induced cardiac injury in rat through down regulation of inflammatory response

2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Najah Hadi ◽  
Nasser Ghaly Yousif ◽  
Fadhil G Al-amran ◽  
Nadhem K Huntei ◽  
Bassim I Mohammad ◽  
...  
Keyword(s):  
Vitamin E ◽  
Inflammatory Response ◽  
Cardiac Injury ◽  
Down Regulation

Interleukin-27 attenuates myocardial injury after ischemia-reperfusion through down-regulation of inflammatory response

2021 ◽  
Vol 9 (1) ◽  
pp. 62-75
Author(s):  
Mai HN ◽  
Lee YS
Keyword(s):  
Inflammatory Response ◽  
Ventricular Function ◽  
Myocardial Injury ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Mice Model ◽  
Down Regulation ◽  
Stat Pathway

The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial injury and inflammatory response is an important process during the pathogenesis of myocardial I/R injury. IL-27, this cytokine is mainly produced by cells of myeloid origin such as monocytes, macrophages, dendritic cells, and microglial cells, in response to stimuli acting through Toll-like receptors. The objective of present study is to assess whether IL-27 can improve ventricular function after myocardial ischemia by down-regulation of inflammatory response. The results demonstrated that the IL-27 markedly attenuated Left Ventricular Function (LVF) in mice model, and reduced plasma level of cTn-I as marker of cardiac injury. Moreover, the IL-27 was associated with up-regulation in both chemokine and cytokines expression following I/R, through down-regulation of activation of JAK/STAT pathway.

scholarly journals Silencing of microRNA-155 in mice during acute inflammatory response leads to derepression of c/ebp Beta and down-regulation of G-CSF

2009 ◽  
Vol 37 (17) ◽  
pp. 5784-5792 ◽  
Author(s):  
Jesper Worm ◽  
Jan Stenvang ◽  
Andreas Petri ◽  
Klaus Stensgaard Frederiksen ◽  
Susanna Obad ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Down Regulation

scholarly journals Thyroxine Affects Lipopolysaccharide-Induced Macrophage Differentiation and Myocardial Cell Apoptosis via the NF-κB p65 Pathway Both In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Shan Zhu ◽  
Yuan Wang ◽  
Hongtao Liu ◽  
Wen Wei ◽  
Yi Tu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cardiac Dysfunction ◽  
Cell Apoptosis ◽  
Cardiac Injury ◽  
Myocardial Cell ◽  
M2 Macrophage ◽  
Mrna Levels ◽  
Cytokine Mrna ◽  
M1 Macrophage

Background. Numerous studies have demonstrated that the inflammatory response is involved in the progression of lipopolysaccharide- (LPS-) induced myocardial cell apoptosis. Accumulating evidence has shown that thyroxine participates in diseases by downregulating the inflammatory response. This study aimed at investigating whether thyroxine alleviates LPS-induced myocardial cell apoptosis. Methods. Bone marrow-derived macrophages (Mø) were treated with LPS and thyroxine, and Mø differentiation and Mø-related cytokine expression were measured. The effect of Mø differentiation on mouse cardiomyocyte (MCM) apoptosis was also detected in vitro. In addition, C57BL/6 mice underwent thyroidectomy and were treated with LPS 35 days later; subsequently, Mø differentiation and myocardial cell apoptosis in hearts were analyzed. To determine whether the nuclear factor-kappa B (NF-κB) p65 pathway mediates the effect of thyroxine on Mø differentiation and myocardial cell apoptosis, the specific NF-κB p65 pathway inhibitor JSH-23 was administered to mice that underwent a thyroidectomy. Results. Levothyroxine treatment significantly reduced the activation of the NF-κB p65 pathway, decreased M1 macrophage (Mø1) differentiation and Mø1-related cytokine mRNA levels in LPS-treated Mø, and increased M2 macrophage (Mø2) differentiation and Mø2-related cytokine mRNA expression. The protective effects of levothyroxine on MCM apoptosis mediated by LPS-treated Mø were alleviated by JSH-23. In mice, thyroidectomy aggravated LPS-induced cardiac injury and cardiac dysfunction, further promoted NF-κB p65 activation, and increased cardiac Mø1 expression and myocardial cell apoptosis but decreased cardiac Mø2 expression. JSH-23 treatment significantly ameliorated the thyroidectomy-induced increases in myocardial cell apoptosis and Mø differentiation. Conclusions. Thyroxine alleviated the Mø1/Mø2 imbalance, reduced the inflammatory response, decreased myocardial cell apoptosis, and protected against cardiac injury and cardiac dysfunction in LPS-treated mice. Thyroxine may be a novel therapeutic strategy to prevent and treat LPS-induced cardiac injury.

scholarly journals Down-Regulation of Glycosylphosphatidylinositol-Specific Phospholipase D Induced by Lipopolysaccharide and Oxidative Stress in the Murine Monocyte- Macrophage Cell Line RAW 264.7

2001 ◽  
Vol 69 (5) ◽  
pp. 3214-3223 ◽  
Author(s):  
Xiaohan Du ◽  
Martin G. Low
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cell Line ◽  
Phospholipase D ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Down Regulation ◽  
Tnf Α

ABSTRACT Serum glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) activity is reduced over 75% in systemic inflammatory response syndrome. To investigate the mechanism of this response, expression of the GPI-PLD gene was studied in the mouse monocyte-macrophage cell line RAW 264.7 stimulated with lipopolysaccharide (LPS; 0.5 to 50 ng/ml). GPI-PLD mRNA was reduced approximately 60% in a time- and dose-dependent manner. Oxidative stress induced by 0.5 mM H2O2 or 50 μM menadione also caused a greater than 50% reduction in GPI-PLD mRNA. The antioxidant N-acetyl-l-cysteine attenuated the down-regulatory effect of H2O2but not of LPS. Cotreatment of the cells with actinomycin D inhibited down-regulation induced by either LPS or H2O2. The half-life of GPI-PLD mRNA was not affected by LPS, or decreased slightly with H2O2, indicating that the reduction in GPI-PLD mRNA is due primarily to transcriptional regulation. Stimulation with tumor necrosis factor alpha (TNF-α) resulted in ∼40% reduction in GPI-PLD mRNA in human A549 alveolar carcinoma cells but not RAW 264.7 cells, suggesting that alternative pathways could exist in different cell types for down-regulating GPI-PLD expression during an inflammatory response and the TNF-α autocrine signaling mechanism alone is not sufficient to recapitulate the LPS-induced reduction of GPI-PLD in macrophages. Sublines of RAW 264.7 cells with reduced GPI-PLD expression exhibited increased cell sensitivity to LPS stimulation and membrane-anchored CD14 expression on the cell surface. Our data suggest that down-regulation of GPI-PLD could play an important role in the control of proinflammatory responses.

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