Peroxisome proliferator‐activated receptor gamma coactivator‐1α/HSF1 axis effectively alleviates lipopolysaccharide‐induced acute lung injury via suppressing oxidative stress and inflammatory response

2018 ◽  
Vol 120 (1) ◽  
pp. 544-551 ◽  
Author(s):  
Xingbo Dang ◽  
Gongliang Du ◽  
Wei Hu ◽  
Longyang Ma ◽  
Pei Wang ◽  
...  
2005 ◽  
Vol 33 (10) ◽  
pp. 2309-2316 ◽  
Author(s):  
Dong Liu ◽  
Bang-Xiong Zeng ◽  
Shi-Hai Zhang ◽  
Yue-Lan Wang ◽  
Lian Zeng ◽  
...  

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Lili Liu ◽  
Junyi Chen ◽  
Xiaofang Zhang ◽  
Xue Cui ◽  
Nana Qiao ◽  
...  

Abstract The present study aims to reveal the molecular mechanism of peroxisome proliferator-activated receptor γ (PPARγ) on sepsis-induced acute lung injury (ALI). To do that, the rat injury model was established using cecal ligation and perforation (CLP) method, followed by different treatments, and the rats were divided into Sham group, CLP group, CLP + rosiglitazone (PPARγ agonist) group, CLP + GW9662 (PPARγ inhibitor) group, CLP + bpV (phosphatase and tensin homolog (PTEN) inhibitor) group, CLP + GW9662 + bpV group. Compared with Sham group, the mRNA and protein expression levels of PPARγ were down-regulated, the inflammation levels were elevated, and the apoptosis was increased in CLP group. After treatment with rosiglitazone, the protein expression level of PPARγ was significantly up-regulated, the phosphorylation level of PTEN/β-catenin pathway was decreased, the PTEN/β-catenin pathway was inhibited, the lung injury, inflammation and apoptosis were reduced. The opposite effect was observed after treatment with GW9662. Besides, bpV inhibited PTEN/β-catenin pathway, and relieved the lung tissue injury. The overexpression of PPARγ reduced inflammatory response and inhibited apoptosis in sepsis-induced ALI. Furthermore, PPARγ relieved the sepsis-induced ALI by inhibiting the PTEN/β-catenin pathway.


Medicina ◽  
2020 ◽  
Vol 56 (8) ◽  
pp. 386 ◽  
Author(s):  
María Elena Soto ◽  
Verónica Guarner-Lans ◽  
Elizabeth Soria-Castro ◽  
Linaloe Manzano Pech ◽  
Israel Pérez-Torres

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes the corona virus disease-19 which is accompanied by severe pneumonia, pulmonary alveolar collapses and which stops oxygen exchange. Viral transmissibility and pathogenesis depend on recognition by a receptor in the host, protease cleavage of the host membrane and fusion. SARS-CoV-2 binds to the angiotensin converting enzyme 2 receptor. Here, we discuss the general characteristics of the virus, its mechanism of action and the way in which the mechanism correlates with the comorbidities that increase the death rate. We also discuss the currently proposed therapeutic measures and propose the use of antioxidant drugs to help patients infected with the SARS-CoV-2. Oxidizing agents come from phagocytic leukocytes such as neutrophils, monocytes, macrophages and eosinophils that invade tissue. Free radicals promote cytotoxicity thus injuring cells. They also trigger the mechanism of inflammation by mediating the activation of NFkB and inducing the transcription of cytokine production genes. Release of cytokines enhances the inflammatory response. Oxidative stress is elevated during critical illnesses and contributes to organ failure. In corona virus disease-19 there is an intense inflammatory response known as a cytokine storm that could be mediated by oxidative stress. Although antioxidant therapy has not been tested in corona virus disease-19, the consequences of antioxidant therapy in sepsis, acute respiratory distress syndrome and acute lung injury are known. It improves oxygenation rates, glutathione levels and strengthens the immune response. It reduces mechanical ventilation time, the length of stay in the intensive care unit, multiple organ dysfunctions and the length of stay in the hospital and mortality rates in acute lung injury/acute respiratory distress syndrome and could thus help patients with corona virus disease-19.


Respiration ◽  
2008 ◽  
Vol 77 (3) ◽  
pp. 311-319 ◽  
Author(s):  
Yasuhiro Aoki ◽  
Toshitaka Maeno ◽  
Kana Aoyagi ◽  
Manabu Ueno ◽  
Fumiaki Aoki ◽  
...  

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