Role of acute‐phase protein ORM in a mice model of ischemic stroke

2019 ◽  
Vol 234 (11) ◽  
pp. 20533-20545 ◽  
Author(s):  
Jing‐Jing Wan ◽  
Peng‐Yuan Wang ◽  
Yu Zhang ◽  
Zhen Qin ◽  
Yang Sun ◽  
...  
1993 ◽  
Vol 265 (4) ◽  
pp. E660-E666 ◽  
Author(s):  
D. Breuille ◽  
M. C. Farge ◽  
F. Rose ◽  
M. Arnal ◽  
D. Attaix ◽  
...  

Sepsis induces metabolic disorders that include loss of body weight, muscle wasting, and acute-phase protein synthesis in liver. Cytokines are generally recognized as active mediators of these disorders, and the implication of tumor necrosis factor (TNF) has been frequently discussed in the recent past. However, the identity of the active agent in alterations of protein metabolism is still controversial. To improve our understanding of the role of cytokines in mediating muscle wasting observed in sepsis, we investigated muscle and liver protein metabolism in the following three groups of rats: infected control rats (INF-C); infected rats pretreated with pentoxifylline (PTX-INF), which is a potent inhibitor of TNF secretion; and pair-fed rats for the PTX-INF group pretreated with pentoxifylline. Pentoxifylline nearly completely suppressed TNF secretion but did not influence the transient fall in rectal temperature, the decreased hematocrit, and the increased liver protein mass and synthesis observed in INF-C rats. Pentoxifylline decreased the anorexia, the loss of body weight and muscle protein observed in INF-C animals, and partially prevented the decrease in muscle protein synthesis induced by infection. The overall data indicate that pentoxifylline is an effective agent in mitigating the characteristic muscle protein wasting induced by sepsis and confirm the limited role of TNF in the mediation of the acute-phase protein synthesis. Our results suggest a probable implication of TNF in the regulation of protein balance in muscle but do not allow discarding possible implication of other mediators that would be inhibited by pentoxifylline.


Author(s):  
Xia-Fang Chen ◽  
Jing Wu ◽  
Yi-Dan Zhang ◽  
Chen-Xing Zhang ◽  
Xu-Ting Chen ◽  
...  

2016 ◽  
Vol 93 ◽  
pp. 93-96 ◽  
Author(s):  
David M. Conrad ◽  
David W. Hoskin ◽  
Robert Liwski ◽  
Christopher Naugler

1997 ◽  
Vol 273 (4) ◽  
pp. E720-E726 ◽  
Author(s):  
Stephen J. Wigmore ◽  
Kenneth C. H. Fearon ◽  
Jean P. Maingay ◽  
Paul B. S. Lai ◽  
James A. Ross

During the course of studies designed to identify the role of cytokines in the reprioritization of hepatic protein synthesis associated with cachexia we detected a hepatocyte-stimulating moiety in the supernatants of pancreatic cancer cells that was unrelated to interleukin (IL)-6. This study identifies that moiety as IL-8 and investigates the role of IL-8 in the induction of acute-phase protein production. The human pancreatic cancer cell line MIA PaCa-2 produced >1 ng/ml of IL-8 per 24 h, and supernatants from this cell line induced C-reactive protein (CRP) production from isolated human hepatocytes. Addition of neutralizing anti-human IL-8 antibody to such supernatants produced almost complete inhibition of CRP production. The addition of recombinant human IL-8 to hepatocytes resulted in a dose-dependent increase in CRP, α1-acid glycoprotein, and α1-antichymotrypsin production and a decrease in the production of transferrin and prealbumin. This study demonstrates that recombinant or tumor-derived IL-8 can modulate acute-phase protein production from isolated human hepatocytes and from human hepatoma cells.


2017 ◽  
Vol 312 (3) ◽  
pp. E183-E189 ◽  
Author(s):  
Angela Szeto ◽  
Ni Sun-Suslow ◽  
Armando J. Mendez ◽  
Rosa I. Hernandez ◽  
Klaus V. Wagner ◽  
...  

It has been demonstrated that the neuropeptide oxytocin (OT) attenuates oxidative stress and inflammation in macrophages. In the current study, we examined the role of inflammation on the expression of the oxytocin receptor (OXTR). We hypothesized that OXTR expression is increased during the inflammation through a nuclear factor-κB (NF-κB)-mediated pathway, thus responding as an acute-phase protein. Inflammation was induced by treating macrophages (human primary, THP-1, and murine) with lipopolysaccharide (LPS) and monitored by expression of IL-6. Expression of OXTR and vasopressin receptors was assessed by qPCR, and OXTR expression was confirmed by immunoblotting. Inflammation upregulated OXTR transcription 10- to 250-fold relative to control in THP-1 and human primary macrophages and increased OXTR protein expression. In contrast, vasopressin receptor-2 mRNA expression was reduced following LPS treatment. Blocking NF-κB activation prevented the increase in OXTR transcription. OT treatment of control cells and LPS-treated cells increased ERK1/2 phosphorylation, demonstrating activation of the OXTR/Gαq/11 signaling pathway. OT activation of OXTR reduced secretion of IL-6 in LPS-activated macrophages. Collectively, these findings suggest that OXTR is an acute-phase protein and that its increased expression is regulated by NF-κB and functions to attenuate cellular inflammatory responses in macrophages.


2020 ◽  
Vol 23 (14) ◽  
Author(s):  
Thamer Jaber Chali ◽  
Husam Oudah ALjwaid ◽  
Ismaeal Sadiq Kashan ◽  
Hashim Raheem Tarish ◽  
Murtadha H. AlJanabi

2005 ◽  
Vol 15 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Guido Bellinghieri ◽  
Domenico Santoro ◽  
Menotti Calvani ◽  
Vincenzo Savica

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