Sinomenine ameliorates septic acute lung injury in mice by modulating gut homeostasis via aryl hydrocarbon receptor/Nrf2 pathway

2021 ◽  
pp. 174581
Author(s):  
Wei Song ◽  
Xiaoting Yang ◽  
Wanqiu Wang ◽  
Zi Wang ◽  
Jie Wu ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Weifeng Yao ◽  
Gangjian Luo ◽  
Guosong Zhu ◽  
Xinjin Chi ◽  
Ailan Zhang ◽  
...  

Objective. This study aimed to investigate whether propofol pretreatment can protect against liver transplantation-induced acute lung injury (ALI) and to explore whether Nrf2 pathway is involved in the protections provided by propofol pretreatment.Method. Adult male Sprague-Dawley rats were divided into five groups based on the random number table. Lung pathology was observed by optical microscopy. Lung water content was assessed by wet/dry ratio, and PaO2was detected by blood gas analysis. The contents of H2O2, MDA, and SOD activity were determined by ELISA method, and the expression of HO-1, NQO1, Keap1, and nuclear Nrf2 was assayed by western blotting.Results. Compared with saline-treated model group, both propofol and N-acetylcysteine pretreatment can reduce the acute lung injury caused by orthotopic autologous liver transplantation (OALT), decrease the lung injury scores, lung water content, and H2O2and MDA levels, and improve the arterial PaO2and SOD activity. Furthermore, propofol (but not N-acetylcysteine) pretreatment especially in high dose inhibited the expression of Keap1 and induced translocation of Nrf2 into the nucleus to further upregulate the expression of HO-1 and NQO1 downstream.Conclusion. Pretreatment with propofol is associated with attenuation of OALT-induced ALI, and the Nrf2 pathway is involved in the antioxidative processes.


2019 ◽  
Vol 111 ◽  
pp. 733-739 ◽  
Author(s):  
Guizhen Zheng ◽  
Huijuan Ren ◽  
Hongqiang Li ◽  
Xiuhua Li ◽  
Tiancao Dong ◽  
...  

Aging ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 13400-13421 ◽  
Author(s):  
Zhaohui Liu ◽  
Yan Li ◽  
Lili Yu ◽  
Yulin Chang ◽  
Jingui Yu

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0196405 ◽  
Author(s):  
Ying Lu ◽  
Ting Yu ◽  
Jingyao Liu ◽  
Lina Gu

2020 ◽  
pp. 153537022096378
Author(s):  
Gabriela Guzmán-Navarro ◽  
Mario Bermúdez de León ◽  
Irene Martín-Estal ◽  
Raquel Cuevas-Díaz Durán ◽  
Laura Villarreal-Alvarado ◽  
...  

Hyperoxia−hypoxia exposure is a proposed cause of alveolar developmental arrest in bronchopulmonary dysplasia in preterm infants, where mitochondrial reactive oxygen species and oxidative stress vulnerability are increased. The aryl hydrocarbon receptor (AhR) is one of the main activators of the antioxidant enzyme system that protects tissues and systems from damage. The present study aimed to determine if the activation of the AhR signaling pathway by prenatal administration of indole-3-carbinol (I3C) protects rat pups from hyperoxia–hypoxia-induced lung injury. To assess the activation of protein-encoding genes related to the AhR signaling pathway ( Cyp1a1, Cyp1b1, Ugt1a6, Nqo1, and Gsta1), pup lungs were excised at 0, 24, and 72 h after birth, and mRNA expression levels were quantified by reverse transcription-quantitative polymerase chain reaction assays (RT-qPCR). An adapted Ratner's method was used in rats to evaluate radial alveolar counts (RACs) and the degree of fibrosis. The results reveal that the relative expression of AhR-related genes in rat pups of prenatally I3C-treated dams was significantly different from that of untreated dams. The RAC was significantly lower in the hyperoxia–hypoxia group (4.0 ± 1.0) than that in the unexposed control group (8.0 ± 2.0; P <  0.01). When rat pups of prenatally I3C-treated dams were exposed to hyperoxia–hypoxia, an RAC recovery was observed, and the fibrosis index was similar to that of the unexposed control group. A cytokine antibody array revealed an increase in the NF-κB signaling cascade in I3C-treated pups, suggesting that the pathway could regulate the inflammatory process under the stimulus of this compound. In conclusion, the present study demonstrates that I3C prenatal treatment activates AhR-responsive genes in pup’s lungs and hence attenuates lung damage caused by hyperoxia–hypoxia exposure in newborns.


2019 ◽  
Vol 60 (10) ◽  
pp. 1760-1768 ◽  
Author(s):  
Meige Sun ◽  
Ning Ma ◽  
Ting He ◽  
Lee J. Johnston ◽  
Xi Ma

2015 ◽  
Vol 148 (1) ◽  
pp. 276-287 ◽  
Author(s):  
Binoy Shivanna ◽  
Shaojie Zhang ◽  
Ananddeep Patel ◽  
Weiwu Jiang ◽  
Lihua Wang ◽  
...  

2020 ◽  
Vol 146 ◽  
pp. 222-233 ◽  
Author(s):  
Xiao-Ting Huang ◽  
Wei Liu ◽  
Yong Zhou ◽  
Mei Sun ◽  
Hui-Hui Yang ◽  
...  

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