Protective effect of taurine on sepsis‑induced lung injury via inhibiting the p38/MAPK signaling pathway

Abstract

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.

Knockdown of CXCL3-inhibited apoptosis and inflammation in lipopolysaccharide-treated BEAS-2B and HPAEC through inactivating MAPKs pathway

“…MAPKs signaling has been shown to be essential for dysregulated and overly aggressive inflammatory response in the development of sepsis. 24 MAPKs were abnormally activated in rats with sepsis-associated acute lung injury, 25 and inhibition in the phosphorylation of p38 and JNK in lung tissues alleviated sepsis-associated acute lung injury. 24 Activation of CXCLs/CXCR2 axis promoted the activation of p38/ERK signaling to regulate cell survival and migration in inflammatory diseases.…”

Protective effects of Descurainia sophia seeds extract and its fractions on pulmonary edema by untargeted urine and serum metabolomics strategy

“…Taurine has been demonstrated to inhibit the lung damage caused by oxidative stress by enhancing the activity of antioxidWWant enzymes in the lung ( Schuller-Levis et al, 1994 ; Abdih et al, 2000 ; Zhao et al, 2018 ). Chen and colleagues discovered that taurine can attenuate sepsis-induced lung injury through anti-inflammatory actions and antioxidative stress, reducing overexpression of tumor necrosis factor (TNF)-α and IL-1β and neutrophil infiltration ( Chen, J. et al, 2021 ). Early studies also showed that abnormalities of the taurine metabolism of occurred in viral pneumonia and lipopolysaccharide-induced pulmonary injury ( Chen, F. et al, 2022 ).…”

Lidocaine ameliorates intestinal barrier dysfunction in irritable bowel syndrome by modulating corticotropin‐releasing hormone receptor 2

“…51 In addition, lidocaine has a protective effect on LPS-induced acute lung injury (ALI) in rats by inhibiting an excessive inflammatory response. 52 In this study, we explored the effect of lidocaine on intestinal barrier function in WAS-induced IBS rats, a widely used model for evaluating drugs targeting intestinal barrier injury. 34 Lidocaine treatment effectively ameliorated IBS-related symptoms in rats, including visceral hypersensitivity, body weight changes, low-level inflammation, and alterations in spleen and thymus index.…”