scholarly journals Hydrogen Gas Presents a Promising Therapeutic Strategy for Sepsis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Keliang Xie ◽  
Lingling Liu ◽  
Yonghao Yu ◽  
Guolin Wang

Sepsis is characterized by a severe inflammatory response to infection. It remains a major cause of morbidity and mortality in critically ill patients despite developments in monitoring devices, diagnostic tools, and new therapeutic options. Recently, some studies have found that molecular hydrogen is a new therapeutic gas. Our studies have found that hydrogen gas can improve the survival and organ damage in mice and rats with cecal ligation and puncture, zymosan, and lipopolysaccharide-induced sepsis. The mechanisms are associated with the regulation of oxidative stress, inflammatory response, and apoptosis, which might be through NF-κB and Nrf2/HO-1 signaling pathway. In this paper, we summarized the progress of hydrogen treatment in sepsis.

Shock ◽  
2000 ◽  
Vol 13 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Daniel G. Remick ◽  
David E. Newcomb ◽  
Gerald L. Bolgos ◽  
Douglas R. Call

2021 ◽  
Vol 49 (5) ◽  
pp. 117-124
Author(s):  
Wenmei Liang ◽  
Li Guo ◽  
Tonghua Liu ◽  
Song Qin

Background: Sepsis is a systemic inflammatory response syndrome and leads to patient’s death. Objective: To investigate the effect of myocyte enhancer factor 2 (MEF2C) on acute lung injury (ALI) with sepsis and its possible mechanism.Material and Methods: The cecal ligation and puncture (CLP)-induced sepsis rat model was established. The lung injury was determined by lung wet–dry weight ratio, the concentration of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), Interlukin (IL)-6, IL-1β, and IL-10, were measured by the enzyme-linked-immunosorbent serologic assay kit. The cell apoptosis was detected by TUNEL staining assay.Results: Interestingly, MEF2C was down-regulated in this model. Moreover, adeno-associated virus (AAV)-MEF2C treatment markedly suppressed TNF-α, IL-1β, and IL-6 concentrations but promoted IL-10 concentration in serum in CLP-challenged rats. Besides, overexpression of MEF2C alleviates CLP-induced lung injury. Interestingly, AAV-MEF2C treatment was confirmed to suppress apoptosis in CLP-induced sepsis rats as well as promote aquaporin APQ1 expres-sion. Mechanistically, the rescue experiments indicated that MEF2C alleviated CLP-induced lung inflammatory response and apoptosis via up-regulating AQP1.Conclusion: In summary, overexpression of MEF2C suppressed CLP-induced lung inflamma-tory response and apoptosis via up-regulating AQP1, providing a novel therapeutic target for sepsis-induced ALI.


2020 ◽  
Author(s):  
Tina Didari ◽  
Maryam Baeeri ◽  
Mahban Rahimifard ◽  
Shilan Mozaffari ◽  
Hamed Haghi-Aminjan ◽  
...  

Abstract Background: Rodent Cecal Ligation and Puncture (CLP) models, which mimic sepsis in humans. Gauges needle size during CLP related to cytokine storm, inflammation and organ failure.This study focus on precise and low cost various biochemical markers to trace sepsis severity in cardiopulmonary system and blood after CLP with gauge needle size -18 (G-18) and -21 (G-21) in rats.Results: For the purpose of this study, 18 male Wistar rats were assigned into three groups: CLP procedure with G-18 needle, CLP procedure with G-21 and sham. Following the procedure, oxidative stress markers, blood markers, apoptosis indicators, gene expression of autophagy and cellular hypoxia and histopathological assessments were carried out in the cardiopulmonary tissue and blood 24 hours after CLP. All measured factors were increased in both G-18 and G-21 gauge groups in comparison with the sham. Moreover, 24 hours after CLP, inflammatory markers, blood profile, lactate level, pro-inflammatory cytokines, caspases, gene expression of cellular homeostasis and autophagy in samples were more pronouncedly increased in the G-18 group in comparison with the G-21. Conclusions: This experiment provides a significant association of inflammation and cytokine storm with anti-oxidant property, apoptotic condition and gene expression of tissue and blood infection related to severity organ damage were increased with G-18 compare to G-21. Our study has identified cost-effective indicators to evaluate organ failure during sepsis. This should be considered by all investigators using G-18 in comparison with G-21 to induce severe sepsis.


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