SN50, a Cell-Permeable Inhibitor of Nuclear Factor-κB, Attenuates Ventilator-Induced Lung Injury in an Isolated and Perfused Rat Lung Model

Shock ◽  
2016 ◽  
Vol 46 (2) ◽  
pp. 194-201 ◽  
Author(s):  
Chih-Feng Chian ◽  
Chi-Huei Chiang ◽  
Chiao-Hui Chuang ◽  
Shiou-Ling Liu ◽  
Chen-Liang Tsai
2014 ◽  
Vol 163 (3) ◽  
pp. 211-220 ◽  
Author(s):  
Chih-Feng Chian ◽  
Chi-Huei Chiang ◽  
Chiao-Hui Chuang ◽  
Shiou-Ling Liu

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2258
Author(s):  
Won-Gun Kwack ◽  
Yoon-Je Lee ◽  
Eun-Young Eo ◽  
Jin-Haeng Chung ◽  
Jae-Ho Lee ◽  
...  

Ventilator-induced lung injury (VILI) is an important critical care complication. Nuclear factor-κB (NF-κB) activation, a critical signaling event in the inflammatory response, has been implicated in the tracking of the lung injury. The present study aimed to determine the effect of simultaneous pretreatment with enteral aspirin and omega-3 fatty acid on lung injury in a murine VILI model. We compared the lung inflammation after the sequential administration of lipopolysaccharides and mechanical ventilation between the pretreated simultaneous enteral aspirin and omega-3 fatty acid group and the non-pretreatment group, by quantifying NF-κB activation using an in vivo imaging system to detect bioluminescence signals. The pretreated group with enteral aspirin and omega-3 fatty acid exhibited a smaller elevation of bioluminescence signals than the non-pretreated group (p = 0.039). Compared to the non-pretreated group, the pretreatment group with simultaneous enteral aspirin and omega-3 fatty acid showed reduced expression of the pro-inflammatory cytokine, tumor necrosis factor-α, in bronchoalveolar lavage fluid (p = 0.038). Histopathological lung injury scores were also lower in the pretreatment groups compared to the only injury group. Simultaneous pretreatment with enteral administration of aspirin and omega-3 fatty acid could be a prevention method for VILI in patients with impending mechanical ventilation therapy.


2011 ◽  
Vol 37 (8) ◽  
pp. 1360-1367 ◽  
Author(s):  
Chi-Huei Chiang ◽  
Chiao-Hui Chuang ◽  
Shiou-Ling Liu ◽  
Tzong-Shyuan Lee ◽  
Yu Ru Kou ◽  
...  

Injury ◽  
2012 ◽  
Vol 43 (8) ◽  
pp. 1257-1263 ◽  
Author(s):  
Chi-Huei Chiang ◽  
Chiao-Hui Chuang ◽  
Shiou-Ling Liu ◽  
Chih-Feng Chian ◽  
Haibo Zhang ◽  
...  

2020 ◽  
Vol 19 (3) ◽  
pp. 255-260
Author(s):  
Fan Yang ◽  
Lu Deng ◽  
MuHu Chen ◽  
Ying Liu ◽  
Jianpeng Zheng

Acute lung injury initiated systemic inflammation leads to sepsis. Septic mice show a series of degenerative changes in lungs as demonstrated by pulmonary congestion, alveolar collapse, inflammatory cell infiltration, and increased wet-todry weight in lungs. 6-Gingerol ameliorates histopathological changes and clinical outcome of the sepsis. The increase in the levels of tumor necrosis factor-α, interleukin-1 beta, interleukin-6, and interleukin-18 in septic mice were reduced by administration with 6-Gingerol. Also, 6-Gingerol attenuates sepsis-induced increase of malonaldehyde and decrease of catalase, superoxide, and glutathione. Enhanced phospho-p65, reduced nuclear factor erythropoietin-2-related factor 2, and heme oxygenase 1 in septic mice were reversed by administration with 6-Gingerol. In conclusion, 6-Gingerol demonstrates anti-inflammatory and antioxidant effects against sepsis associated acute lung injury through inactivation of nuclear factor-kappa B and activation of nuclear-factor erythroid 2-related factor 2 pathways.


2002 ◽  
Vol 124 (6) ◽  
pp. 1137-1144 ◽  
Author(s):  
Marc de Perrot ◽  
Yumiko Imai ◽  
George A. Volgyesi ◽  
Thomas K. Waddell ◽  
Mingyao Liu ◽  
...  

2009 ◽  
Vol 160 (2) ◽  
pp. 283-292 ◽  
Author(s):  
S. Tanaka ◽  
S. Nishiumi ◽  
M. Nishida ◽  
Y. Mizushina ◽  
K. Kobayashi ◽  
...  

2017 ◽  
Vol 82 (3) ◽  
pp. 566-574 ◽  
Author(s):  
Seok Ho Choi ◽  
Gil Joon Suh ◽  
Woon Yong Kwon ◽  
Kyung Su Kim ◽  
Min Ji Park ◽  
...  

2001 ◽  
Vol 280 (3) ◽  
pp. L400-L408 ◽  
Author(s):  
Casey M. Calkins ◽  
Denis D. Bensard ◽  
Julie K. Heimbach ◽  
Xianzhong Meng ◽  
Brian D. Shames ◽  
...  

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-κB (NF-κB), an inducible transcription factor under the control of inhibitory factor κB-α (IκB-α). We have previously demonstrated that l-arginine (l-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized thatl-Arg would attenuate the production of lung chemokines by stabilizing IκB-α and preventing NF-κB DNA binding. We examined the effect of l-Arg on chemokine production, IκB-α degradation, and NF-κB DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was given before l-Arg. LPS induced the production of chemokine protein and mRNA. l-Arg attenuated the production of chemokine protein and mRNA, prevented the decrease in IκB-α levels, and inhibited NF-κB DNA binding. NO synthase inhibition abolished the effects of l-Arg on all measured parameters. Our results suggest that l-Arg abrogates chemokine protein and mRNA production in rat lung after LPS. This effect is dependent on NO and is mediated by stabilization of IκB-α levels and inhibition of NF-κB DNA binding.


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