scholarly journals Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress

2020 ◽  
Vol Volume 13 ◽  
pp. 4179-4190
Author(s):  
Ke Wei ◽  
Jie Luo ◽  
Jun Cao ◽  
Lihua Peng ◽  
Li Ren ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress ◽  
Obese Rats

scholarly journals Endoplasmic Reticulum Stress of Neutrophils Is Required for Ischemia/Reperfusion–Induced Acute Lung Injury

2015 ◽  
Vol 195 (10) ◽  
pp. 4802-4809 ◽  
Author(s):  
Rong Hu ◽  
Zhi-Feng Chen ◽  
Jia Yan ◽  
Qi-Fang Li ◽  
Yan Huang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress ◽  
Ischemia Reperfusion

scholarly journals A Melanin-like Nanoenzyme for Acute Lung Injury Therapy via Suppressing Oxidative and Endoplasmic Reticulum Stress Response

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1850
Author(s):  
Xue-Fang Lou ◽  
Chen Wang ◽  
Ju-Cong Zhang ◽  
Yong-Zhong Du ◽  
Xiao-Ling Xu
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Stress Response ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress ◽  
Therapeutic Effect ◽  
Neutrophil Infiltration ◽  
Endoplasmic Reticulum Stress Response ◽  
Ros Scavenging

Nanoenzyme-mediated catalytic activity is emerging as a novel strategy for reactive oxygen species (ROS) scavenging in acute lung injury (ALI) treatment. However, one of the main hurdles for these metal-containing nanoenzymes is their potential toxicity and single therapeutic mechanism. Herein, we uncovered a melanin-like nanoparticles derived from the self-polymerization of 1,8-dihydroxynaphthalene (PDH nanoparticles), showing a significant anti-inflammation therapeutic effect on ALI mice. The prepared PDH nanoparticles rich in phenol groups could not only act as radical scavengers to alleviate oxidative stress but could also chelate calcium overload to suppress the endoplasmic reticulum stress response. As revealed by the therapeutic effect in vivo, PDH nanoparticles significantly prohibited neutrophil infiltration and the secretion of proinflammatory cytokines (TNF-α and IL-6), thus improving the inflammatory cascade in the ALI model. Above all, our work provides an effective anti-inflammatory nanoplatform by using the inherent capability of melanin-like nanoenzymes, proposing the potential application prospects of these melanin-like nanoparticles for acute inflammation-induced injury treatment.

Hydrogen alleviates hyperoxic acute lung injury related endoplasmic reticulum stress in rats through upregulation of SIRT1

2017 ◽  
Vol 51 (6) ◽  
pp. 622-632 ◽  
Author(s):  
Qiang Sun ◽  
Wenjie Han ◽  
Huijun Hu ◽  
Danfeng Fan ◽  
Yanbo Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress

Ghrelin ameliorates acute lung injury induced by oleic acid via inhibition of endoplasmic reticulum stress

Life Sciences ◽  
2018 ◽  
Vol 196 ◽  
pp. 1-8 ◽  
Author(s):  
Xiuli Tian ◽  
Zhijun Liu ◽  
Ting Yu ◽  
Haitao Yang ◽  
Linlin Feng
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress

scholarly journals The Role of Oxymatrine in Amelioration of Acute Lung Injury Subjected to Myocardial I/R by Inhibiting Endoplasmic Reticulum Stress in Diabetic Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yongpan Huang ◽  
Xian Long ◽  
Xinliang Li ◽  
Saihua Li ◽  
Jianbin He
Keyword(s):  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Troponin ◽  
Diabetic Rats ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Expression Levels ◽  
Creatine Kinase Mb

Background. Oxymatrine (OMT) is the primary pharmacological component of Sophora flavescens Aiton., which has been shown to possess potent antifibrotic, antioxidant, and anti-inflammatory activities. The aim of the present study was to clarify the protective mechanism of OMT on acute lung injury (ALI) subjected to myocardial ischemia/reperfusion (I/R). Methods. A myocardial I/R-induced ALI model was achieved in diabetic rats by occluding the left anterior descending coronary artery for 1 h, followed by reperfusion for 1 h. The levels of inflammatory factors (tumor necrosis factor-α, interleukin- (IL-) 6, and IL-17) in bronchoalveolar lavage fluid were assessed using commercially available kits. The index of myocardial injury, including the detection of cardiac troponin I (cTnI), cardiac troponin T (cTnT), lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB), was also determined using commercially available kits. Hematoxylin and eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to identify histological changes. The expression levels of endoplasmic reticulum chaperone BiP (GRP78), DNA damage-inducible transcript 3 protein (CHOP), eukaryotic translation initiation factor 2-alpha kinase 3 (PERK), inositol dependent enzyme 1α (IRE1α), ATF6, caspase-3, -9, and-12, Bcl-2, and Bax were determined by Western blotting. The mRNA expression levels of GRP78 and CHOP were detected by reverse transcription-quantitative PCR. Results. Myocardial I/R increased the levels of cTnI, cTnT, LDH, and CK-MB in diabetic rats. Damaged and irregularly arranged myocardial cells were also observed, as well as more serious ALI with higher lung injury scores and WET/DRY ratios and lower PaO2. Moreover, the expression of key proteins of endoplasmic reticulum stress (ERS) was increased by I/R injury, including phosphorylated- (p-) PERK, p-IRE1ɑ, and ATF6, as well as decreased levels of apoptosis. These effects were all significantly reversed by OMT treatment. Conclusions. OMT protects against ALI subjected to myocardial I/R by inhibiting ERS in diabetic rats.

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