Sepsis, a leading cause of acute lung injury (ALI), is characterized by an overwhelming systemic inflammatory response and widespread organ injury, particularly in the lungs. Taurine, an intracellular free amino acid, has been used for the treatment of various diseases, including lung injury; however, the underlying mechanisms are unclear. The present study aimed to investigate the protective effect of taurine on septic ALI and the underlying mechanism. A septic ALI model was established by performing cecal ligation and puncture (CLP) surgery on Sprague Dawley rats. Following successful model establishment, rats were treated with taurine. The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats. In addition, compared with that in the ALI group, western blotting results indicated that taurine ameliorated lung epithelial injury by significantly increasing the expression levels of lung epithelial markers, E-cadherin and occludin. The western blotting results demonstrated that, compared with the control group, the p38/MAPK and NF-κB signaling pathways were significantly activated in CLP-induced septic ALI model rats, but taurine significantly suppressed ALI-mediated signaling pathway activation. To investigate the mechanism underlying taurine in the treatment of septic ALI, CLP-induced septic ALI model rats were treated with an antagonist of the p38/MAPK signaling pathway (SB203580). The effects of SB203580 on CLP-induced septic ALI model rats were similar to those of taurine. SB203580 significantly attenuated sepsis-induced lung injury and increases in IL-1β and TNF-α concentrations in the lung tissue. In addition, SB203580 promoted restoration of the injured lung tissue and respiratory function in CLP-induced septic ALI model rats. The western blotting results indicated that SB203580 significantly decreased the ratios of phosphorylated (p)-p38/p38 and p-p65/065, and increased the protein expression levels of E-cadherin and occludin compared with those in the ALI group. In summary, the present study demonstrated that taurine alleviated sepsis-induced lung injury, which was associated with suppression of the inflammatory response and oxidative stress via inhibiting the p38/MAPK signaling pathway. Therefore, the p38/MAPK signaling pathway may serve as a potential therapeutic target for the treatment of sepsis-induced ALI.
Carbon Capture, Utilization and Storage (CCUS) technology is one of the most practical means to meet zero greenhouse gas emission goal of the Paris Agreement and to ensure profitability, which could achieve permanent sequestration of CO2. Due to the cost constraints of CCUS implementation, improving recovery and maximizing storage efficiency have become a critical part of ensuring economic efficiency. This research aims to analyze the effects of key factors on enhancing gas recovery and storage efficiency, combined with the validation of CO2 displacement and storage mechanisms. Therefore, long core experiments and different dimensional simulations were established based on R gas reservoir (one of the actual gas reservoirs in Northeast China), which were designed for sensitivity analyses of different influencing parameters and quantitative analyses of different storage mechanisms during CCUS process. When the conditions (temperature and pressure) were closer to the CO2 critical point, when the following parameters (the CO2 purity, the injection rate and the dip angle) became larger, when the reservoir rhythm was reversed and when the irreducible water was is in existence, the final displacement and storage effects became better because of weaker diffusion, stronger gravity segregation and slower CO2 breakthrough. The contributions of different storage mechanisms were quantified: 83.78% CO2 existed as supercritical fluid; 12.67% CO2 was dissolved in brine; and 3.85% CO2 reacted with minerals. Some supercritical and dissolved CO2 would slowly transform to solid precipitation over time. This work could provide theoretical supports for CCUS technology research and references for CCUS field application. At the same time, countries should further improve CCUS subsidy policies and make concerted efforts to promote the globalization and commercialization of CO2 transport.
Erythropoietin (EPO) has antiapoptotic, antioxidative, and anti-inflammatory effects on ischemia tissues and protects against acute lung injury (ALI) induced by ischemia-reperfusion (I/R). p38 mitogen-activated protein kinases (p38 MAPK) signaling is involved in the processes of I/R-induced ALI. However, the interaction of EPO with p38 MAPK signaling in I/R-induced ALI has not been reported. To explore this issue, we constructed an I/R-induced ALI model in vivo and in vitro using Sprague Dawley rats and BEAS-2B cells. Some I/R rats and hypoxia-reoxygenation (H/R)–induced cells were treated with EPO, and the others were used as control groups. The injuries of lung tissues and cells were respectively assessed by inflammatory cytokine, morphologic changes, cell viability, apoptosis, and oxidative damage–related factors. Western blot determined key proteins in the p38 MAPK signaling. Results indicated that I/R induced the increase of inflammatory factors, lung weight, filtration coefficient, bronchoalveolar lavage fluid protein content, apoptosis, neutrophil, and lung peroxidation, and H/R caused cell growth inhibition, apoptosis, and oxidative damage-related factors’ release. EPO attenuated I/R-induced injury in vivo and in vitro. Furthermore, the increase of p-p38, p-JNK, and p-ERK1/2 in lung tissues and cells induced by I/R was downregulated by EPO. Moreover, both EPO and an inhibitor of p38 MAPK (SB203580) alleviated H/R-induced cell injury. Erythropoietin along with SB203580 had more obvious protection effects than EPO alone. Collectively, EPO alleviated I/R-induced ALI by blocking p38 MAPK signaling. The interaction mechanism of EPO with p38 MAPK signaling contributes to understanding the processes of I/R-induced ALI and provides new insights for the disease treatment.
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