scholarly journals Colony-forming cells reduced the lung injury induced by cardiopulmonary bypass

2020 ◽  
Author(s):  
haibin sun ◽  
Xiaoqing Zhao ◽  
Qihang Tai ◽  
Guangxiao Xu ◽  
Yingnan Ju ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiopulmonary Bypass ◽  
Stress Response ◽  
Lung Injury ◽  
Lung Tissue ◽  
Peripheral Blood ◽  
Capillary Permeability ◽  
Oxidative Stress Response ◽  
Pulmonary Capillary ◽  
Related Proteins

Abstract Background Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pretreated ECFCs. After 24 hours of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight, was evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results After CPB, all the data deteriorated compared with those obtained in the S group. Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2 . Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Conclusions ECFCs significantly reduced lung injury induced by inflammation after CPB.

scholarly journals Endothelial  colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

2020 ◽  
Author(s):  
Haibin Sun ◽  
Xiaoqing Zhao ◽  
Qihang Tai ◽  
Guangxiao Xu ◽  
Yingnan Ju ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Lung Tissue ◽  
Capillary Permeability ◽  
Dry Weight ◽  
Oxidative Stress Response ◽  
Protein Levels ◽  
Endothelial Colony Forming Cells ◽  
Pulmonary Capillary ◽  
Related Proteins

Abstract Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pretreated ECFCs. After 24 hours of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight, was evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score: 1.62±0.51 vs 5.37±0.91 vs 3.37±0.89 vs 4.37±0.74; PaO 2 /FiO 2 : 389±12 vs 233±36 vs 338±28 vs 287±30; wet/dry weight: 3.11±0.32 vs 6.71±0.73 vs 4.66±0.55 vs 5.52±0.57; protein levels: 134±22 vs 442±99 vs 225±41 vs 337±53, all P<0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2 . Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

scholarly journals Lipoxin A4 Reduces Ventilator-Induced Lung Injury in Rats with Large-Volume Mechanical Ventilation

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Qi Wang ◽  
Guang-xiao Xu ◽  
Qi-hang Tai ◽  
Yan Wang
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Lung Tissue ◽  
Capillary Permeability ◽  
Dry Weight ◽  
Oxidative Stress Response ◽  
Lipoxin A4 ◽  
Protein Levels ◽  
Ventilator Induced Lung Injury ◽  
Expression And Activity

Ventilator-induced lung injury (VILI) is a severe and inevitable complication in patients who require mechanical ventilation (MV) for respiratory support. Lipoxin A4 is an endogenous anti-inflammatory and antioxidant mediator. The present study determined the effects of lipoxin A4 on VILI. Twenty-four rats were randomized to the sham, VILI, and lipoxin A4 (LX4) groups. The rats in the VILI and LX4 groups received large-volume MV for 4 hours to simulate VILI. Capillary permeability was evaluated using the PaO2/FiO2 ratio, lung wet/dry weight ratio, and protein level in the lung. VILI-induced inflammation was assessed by measuring cytokines in serum and lung tissue, the expression and activity of NF-κB, and phosphorylated myosin light chain. The oxidative stress response, lung tissue injury, and apoptosis in lung tissue were also estimated, and the expression of apoptotic proteins was examined. MV worsened all of the indices compared to the sham group. Compared to the VILI group, the LX4 group showed significantly improved alveolar-capillary permeability (increased PaO2/FiO2 and decreased wet/dry weight ratios and protein levels), ameliorated histological injury, and reduced local and systemic inflammation (downregulated proinflammatory factors and NF-κB expression and activity). Lipoxin A4 notably inhibited the oxidative stress response and apoptosis and balanced apoptotic protein levels in lung tissue. Lipoxin A4 protects against VILI via anti-inflammatory, antioxidant, and antiapoptotic effects.

scholarly journals Maresin 1 Attenuates Ventilator-induced Lung Injury by Reducing Oxidative Stress through the Nrf2/HO-1 and NF-κB Pathways

2021 ◽  
Author(s):  
Fuquan Wang ◽  
Guangtao Pan ◽  
Jingxu Wang ◽  
Haifa Xia ◽  
Shanglong Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Stress Response ◽  
Lung Injury ◽  
Medical Problem ◽  
Oxidative Stress Response ◽  
Lung Damage ◽  
Positive Role ◽  
Airway Patency ◽  
Oxidative Stress Pathway

Abstract Mechanical ventilation could support the lives of patients with respiratory failure in a variety of ways, including maintaining airway patency and improving oxygenation, etc. However, mechanical ventilation itself could lead to lung damage, which is called mechanical ventilation-related lung injury (VILI). The incidence of VILI is high and the prognosis is poor, so clarifying the mechanism of VILI and seeking effective preventive and therapeutic measures are the urgent medical problem to be resolved. By constructing the VILI model, we studied the effect of Maresin1 on VILI and explored its possible mechanism at the animal level. We tested the related indicators of lung injury, the oxidative stress response, and the inflammatory response. The results indicated that Maresin1 could inhibit the oxidative stress response and excessive inflammation, thus ameliorating lung injury in VILI. We also detected the expression levels of the principal oxidative stress pathway Nrf2 / HO-1 and the key inflammatory transcription factor NF-κB. We used the HO-1 inhibitor ZnPP to further confirm our conclusion. Our results suggested for the first time that Maresin1 could promote the activation of the Nrf2 / HO-1 pathway and significantly suppress the expression of NF-κB to exert a positive role in VILI.

scholarly journals Modulation of the oscillatory mechanics of lung tissue and the oxidative stress response induced by arginase inhibition in a chronic allergic inflammation model

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Luciana RCRB Aristoteles ◽  
Renato F Righetti ◽  
Nathalia Montouro Pinheiro ◽  
Rosana B Franco ◽  
Claudia M Starling ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Lung Tissue ◽  
Allergic Inflammation ◽  
Oxidative Stress Response ◽  
Inflammation Model

scholarly journals Diannexin Can Ameliorate Acute Respiratory Distress Syndrome in Rats by Promoting Heme Oxygenase-1 Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Ying-nan Ju ◽  
Qi-hang Tai ◽  
Guang-xiao Xu ◽  
Xiao-qing Zhao ◽  
Hai-bin Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Lung Tissue ◽  
Distress Syndrome ◽  
Weight Ratio ◽  
Dry Weight ◽  
Oxidative Stress Response ◽  
Heme Oxygenase 1 ◽  
Protein Levels ◽  
Alveolar Capillary

Background. The recombinant protein diannexin can inhibit platelet-mediated events, which contribute to acute respiratory distress syndrome (ARDS). Here, we investigated the effect of diannexin and its effect on heme oxygenase-1 (HO-1) in ARDS. Methods. A total of 32 rats were randomized into sham, ARDS, diannexin (D), and diannexin+HO-1 inhibitor (DH) groups. Alveolar-capillary permeability was evaluated by testing the partial pressure of oxygen to fraction of inspired oxygen (PaO2/FiO2) ratio, lung wet/dry weight ratio, and protein levels in the lung. Inflammation was assessed by measuring cytokine levels in the bronchial alveolar lavage fluid (BALF) and serum and nuclear factor-κB (NF-κB) in the lung tissue. Inducible nitric oxide synthase (iNOS), malondialdehyde (MDA), and myeloperoxidase (MPO) were measured to evaluate the oxidative stress response. Lung tissue pathology and apoptosis were also evaluated. We measured HO-1 expression in the lung tissue to investigate the effect of diannexin on HO-1 in ARDS. Results. Compared with the ARDS group, diannexin improved PaO2/FiO2, lung wet/dry weight ratio, and protein levels in the BALF and decreased levels of cytokines and NF-κB in the lung and serum. Diannexin inhibited the oxidative stress response and significantly ameliorated pathological lung injury and apoptosis. The partial reversal of diannexin effects by a HO-1 inhibitor suggests that diannexin may promote HO-1 expression to ameliorate ARDS. Conclusions. We showed that diannexin can improve alveolar-capillary permeability, inhibit the oxidative stress response and inflammation, and protect against ARDS-induced lung injury and apoptosis.

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