Ethyl pyruvate decreases airway neutrophil infiltration partly through a high mobility group box 1-dependent mechanism in a chemical-induced murine asthma model

2014 ◽  
Vol 21 (1) ◽  
pp. 163-170 ◽  
Author(s):  
Haixiong Tang ◽  
Haijin Zhao ◽  
Jiafu Song ◽  
Hangming Dong ◽  
Lihong Yao ◽  
...  
2015 ◽  
Vol 240 (11) ◽  
pp. 1490-1499 ◽  
Author(s):  
Shan Chen ◽  
Yanjun Wang ◽  
Guoqing Gong ◽  
Jianjun Chen ◽  
Yongzhi Niu ◽  
...  

Diabetes ◽  
2010 ◽  
Vol 59 (6) ◽  
pp. 1496-1505 ◽  
Author(s):  
F. Biscetti ◽  
G. Straface ◽  
R. De Cristofaro ◽  
S. Lancellotti ◽  
P. Rizzo ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Xingfen Su ◽  
Handong Wang ◽  
Jinbing Zhao ◽  
Hao Pan ◽  
Lei Mao

Ethyl pyruvate (EP) has demonstrated neuroprotective effects against acute brain injury through its anti-inflammatory action. The nuclear protein high-mobility group box 1 (HMGB1) can activate inflammatory pathways when released from dying cells. This study was designed to investigate the protective effects of EP against secondary brain injury in rats after Traumatic Brain Injury (TBI). Adult male rats were randomly divided into three groups: (1) Sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + EP group (n=30per group). Right parietal cortical contusion was made by using a weight-dropping TBI method. In TBI + EP group, EP was administered intraperitoneally at a dosage of 75 mg/kg at 5 min, 1 and 6 h after TBI. Brain samples were harvested at 24 h after TBI. We found that EP treatment markedly inhibited the expressions of HMGB1 and TLR4, NF-κB DNA binding activity and inflammatory mediators, such as IL-1β, TNF-αand IL-6. Also, EP treatment significantly ameliorated beam walking performance, brain edema, and cortical apoptotic cell death. These results suggest that the protective effects of EP may be mediated by the reduction of HMGB1/TLR4/NF-κB-mediated inflammatory response in the injured rat brain.


2009 ◽  
Vol 110 (6) ◽  
pp. 1279-1286 ◽  
Author(s):  
Qiang Wang ◽  
Qian Ding ◽  
Yiming Zhou ◽  
Xingchun Gou ◽  
Lichao Hou ◽  
...  

Background Ethyl pyruvate (EP) has been reported to offer a protective effect against ischemic injury through its antiinflammatory action. The nuclear protein high-mobility group box 1 (HMGB1) can activate inflammatory pathways when released from ischemic cells. This study was designed to investigate the neuroprotective effect of EP against spinal cord ischemic injury and the potential role of HMGB1 in this process. Methods EP was administered at various time points before or after 20 min of spinal cord ischemia in male New Zealand rabbits. All animals were sacrificed at 72 h after reperfusion with modified Tarlov criteria, and the spinal cord segment (L4) was harvested for histopathological examination and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining. The HMGB1 levels in serum and spinal cord tissue were analyzed by enzyme-linked immunosorbent assay. Results The treatment of EP at 30 min before ischemia or at 6 h after reperfusion significantly improved the hind-limb motor function scores and increased the numbers of normal motor neurons, which was accompanied with reduction of the number of apoptotic neurons and levels of HMGB1 in serum and spinal cord tissue. The HMGB1 contents of spinal cord tissue correlated well with the numbers of apoptotic motor neurons in the anterior spinal cord at 72 h after reperfusion. Conclusion These results suggest that EP affords a strong protection against the transient spinal cord ischemic injury with a wide therapeutic window through inhibition of HMGB1 release.


2019 ◽  
Vol 23 (8) ◽  
pp. 5679-5691 ◽  
Author(s):  
Yung‐Yang Liu ◽  
Ning‐Hung Chen ◽  
Chih‐Hao Chang ◽  
Shih‐Wei Lin ◽  
Kuo‐Chin Kao ◽  
...  

2003 ◽  
Vol 170 (7) ◽  
pp. 3890-3897 ◽  
Author(s):  
Beatriz Rendon-Mitchell ◽  
Mahendar Ochani ◽  
Jianhua Li ◽  
Jialian Han ◽  
Hong Wang ◽  
...  

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