scholarly journals Additive bone-protective effects of anabolic treatment when used in conjunction with RANKL and tumor necrosis factor inhibition in two rat arthritis models

2005 ◽  
Vol 52 (5) ◽  
pp. 1604-1611 ◽  
Author(s):  
Georg Schett ◽  
Scot Middleton ◽  
Brad Bolon ◽  
Marina Stolina ◽  
Heather Brown ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Protective Effects ◽  
Arthritis Models ◽  
Tumor Necrosis Factor Inhibition ◽  
Anabolic Treatment ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor, tumor necrosis factor inhibition, and cancer risk

2015 ◽  
Vol 31 (3) ◽  
pp. 557-574 ◽  
Author(s):  
Hervé Lebrec ◽  
Rafael Ponce ◽  
Bradley D. Preston ◽  
Jan Iles ◽  
Teresa L. Born ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Cancer Risk ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Inhibition ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor inhibition attenuates white matter gliosis after systemic inflammation in preterm fetal sheep

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Robert Galinsky ◽  
Simerdeep K. Dhillon ◽  
Justin M. Dean ◽  
Joanne O. Davidson ◽  
Christopher A. Lear ◽  
...  
Keyword(s):  
White Matter ◽  
Tumor Necrosis Factor ◽  
Systemic Inflammation ◽  
Tumor Necrosis ◽  
Fetal Sheep ◽  
Tumor Necrosis Factor Inhibition ◽  
Necrosis Factor

scholarly journals Infliximab alleviates the mortality, mesenteric hypoperfusion, aortic dysfunction, and multiple organ damage in septic rats

2017 ◽  
Vol 95 (7) ◽  
pp. 866-872 ◽  
Author(s):  
Erdem Kamil Ozer ◽  
Mustafa Tugrul Goktas ◽  
Ibrahim Kilinc ◽  
Aysun Toker ◽  
Hulagu Bariskaner ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Organ Damage ◽  
Multiple Organ ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Mesenteric Perfusion ◽  
Necrosis Factor

Tumor necrosis factor-alpha (TNF-α) is a pivotal mediator that triggers inflammatory process, oxidative stress, and multiple organ injury in sepsis. We investigated the effects of infliximab on survival, mesenteric artery blood flow (MBF), vascular reactivity, and oxidative and inflammatory injuries in cecal ligation and puncture (CLP)-induced sepsis. Wistar rats were divided into Sham, CLP, Sham+infliximab, and CLP+infliximab subgroups. Twenty-four hours before the operations, rats were injected intraperitoneally with infliximab (7 mg/kg) or vehicle (saline; 1 mL/kg). Twenty hours after the operations, MBF and phenylephrine responses of isolated aortic rings were measured. Tissue damages were examined biochemically and histopathologically. Furthermore, survival rates were monitored throughout 96 h. Infliximab improved survival, mesenteric perfusion, and aortic function after CLP. Increases of serum AST, ALT, LDH, BUN, Cr, and inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6) induced by CLP were blocked by infliximab. Infliximab prevented malondialdehyde elevations in septic liver, lung, spleen, and kidney tissues, as well as glutathione reductions in septic liver, spleen, and kidney tissues. Protective effects of infliximab on multiple organ damage were also observed histopathologically. Infliximab showed protective effects in sepsis due to its improvement effects on mesenteric perfusion, aortic function, and its anti-inflammatory and antioxidative effects.

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