Anti-inflammatory and anti-fibrotic treatment in a rodent model of acute lung injury induced by sulfur dioxide

Wigenstam, Elisabeth; Elfsmark, Linda; Ågren, Lina; Akfur, Christine; Bucht, Anders; Jonasson, Sofia

doi:10.1080/15563650.2018.1479527

Cited by 12 publications

(6 citation statements)

References 43 publications

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“…These changes are consistent with the pathological process of acute lung injury and once again confirmed that sepsis can be caused by acute lung injury. Endogenous sulfur dioxide may play a protective role in lung injury as found in previous studies [19]. In this study, after the endogenous SO 2 donor Na 2 SO 3 /NaHSO 3 was given, the lung tissue structure, lung capillary permeability, and the obvious thickening of the alveolar compartment were all improved; the wet weight/ dry weight ratio of lung tissue and the histology of lung injury was improved.…”

Section: Discussionsupporting

confidence: 76%

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Liu

Gao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. To explore the regulation of endogenous sulfur dioxide on oxidative stress in lung injury induced by sepsis. Method. Forty male Sprague Dawley rats were divided into control, sepsis, sepsis + SO2, and SO2 group randomly used to observe survival rate. The other group of twenty-eight rats were randomly divided as the same manner for mechanism research. The number of WBCS and the percentage of PMN cells were calculated. The microphotographs of morphological changes and the index of quantitative assessment (IQA) of lung tissues were calculated. The ratio of wet/dry (W/D) of lung tissues was calculated. Levels of H2O2, MDA, NO, MPO, SOD, GSH-px, and TNF-α in plasma and lung tissues were measured. Result. The number of WBCS and the percentage of PMN cells decreased in sepsis ( p all < 0.05), and rebound in sepsis+SO2 ( p all < 0.05). The IQA and W/D of lung tissues increased in sepsis ( p for W / D < 0.05 ), and decreased in sepsis+SO2 ( p all < 0.05). H2O2 and MDA of plasma and lung tissues increased in sepsis ( p all < 0.05) and rebound in sepsis+SO2 ( p for H2O2 of plasma and lung tissues <0.05). NO and MPO of plasma and lung tissues increased in sepsis ( p for NO and MPO of lung tissues <0.05) and rebound in sepsis+SO2 ( p all < 0.05 ). SOD of plasma and lung tissues in sepsis group decreased ( p all <0.05) and increased in sepsis+SO2 ( p all < 0.05). GSH-px of plasma and lung tissues decreased in sepsis ( p for plasma <0.05) and increased in sepsis+SO2 ( p for GSH-px of lung tissues <0.05). TNF-α of plasma and lung tissues increased in sepsis ( p all<0.05) and decreased in sepsis+SO2 ( p for lung tissue <0.05). Conclusion. Endogenous sulfur dioxide improves the survival rate of sepsis by improving the oxidative stress response during lung injury.

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Section: Discussionsupporting

confidence: 76%

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Liu

Gao

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Wigenstam et al. (2018) also reported that rats exposed to SO 2 showed labored breathing and decreased bodyweight.…”

Section: Discussionmentioning

confidence: 95%

“…The body weight of male mice was significantly reduced by SO 2 . Wigenstam et al (2018) also reported that rats exposed to SO 2 showed labored breathing and decreased bodyweight.…”

Section: Effect Of Ebn On the Immunological Function Of Mice With Lun...mentioning

confidence: 92%

Edible bird's nest inhibits the inflammation and regulates the immunological balance of lung injury mice by SO₂

et al. 2022

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The purpose was to investigate effect of edible bird's nest (EBN) on the immunological properties of mice with lung injury induced by sulfur dioxide (SO 2 ). In mice, SO 2 exposure caused symptoms that included a cough, tiredness, and weight loss. Administering EBN improved the immunological function of mice with lung injury in a dosedependent manner, leading to recovery of the lung tissue and increasing thymus and spleen indices. IL-2 and IFN-γ in the serum by Th1 cells in response to EBN played a leading role in cellular immune regulation. Moreover, a medium dose of EBN regulated the immune stress response, inhibited apoptosis of splenic lymphocytes, and promoted cellular immunity. EBN inhibited production of IL-8 and MDA and upregulated mRNA expression of atrophin-1 and cyclooxygenase-2 in lung tissue. EBN attenuates the lung injury induced by SO 2 in mice through a mechanism that involves the inhibition of inflammation and regulation of immunological balance.

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“…Wigenstam et al conducted a study in 2018 and observed that, with some mucosal damage occurring to a lesser degree, there was no pulmonary edema. In addition, the development of fibrosis was inhibited compared to the control group, as revealed by the histopathological examination of the tissues collected from the subjects treated with three doses of 200 mg/kg intraperitoneal pirfenidone after inducing iatrogenic pulmonary damage by sulfur dioxide.…”

Section: Discussionmentioning

confidence: 99%

Prevention of tracheal stenosis with pirfenidone after tracheotomy: An experimental study

Türkmen

Pata

2018

The Laryngoscope

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Objectives In this study, pirfenidone's role about reducing tracheal stenosis by suppressing fibrosis and inflammation was examined. Methods Tracheotomy was performed on 14 rats, and their cannulas were fixed to tracheotomy area by stoma suture. Two working groups were established. Rats in the first group were given 15 mg/kg/day (1 mL pirfenidone solution) pirfenidone intraperitoneally for 10 days. In the second group as a control group, 1 mL saline solution was applied intraperitoneally. Ten days later, rats were decanulated and kept alive for 3 more weeks. Anesthetized rats were sacrificed on day 30. All rat tracheas were resected between the first and seventh rings. Epithelial damage, inflammation, and fibrosis were determined histopathologically; diameters of intratracheal lumen and their mucosal thickness parameters were determined histomorphometrically; and TGFβ‐1 (the growth factor beta), TNFα (tumor necrosis factor alpha), and IL‐1β (Interleukin‐1 beta) values were determined immunohistochemically. Results According to the parameters of the control group, fibrosis; diameters of intratracheal lumen; and values of TGFβ‐1, TNFα, and IL‐1β were found to be statistically significant. Conclusion In our study, it was found that pirfenidone reduces fibrosis and narrowing of intratracheal lumen diameter significantly. Level of Evidence NA Laryngoscope, 129:E178–E186, 2019

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Anti-inflammatory and anti-fibrotic treatment in a rodent model of acute lung injury induced by sulfur dioxide

Cited by 12 publications

References 43 publications

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Edible bird's nest inhibits the inflammation and regulates the immunological balance of lung injury mice by SO₂

Prevention of tracheal stenosis with pirfenidone after tracheotomy: An experimental study

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Anti-inflammatory and anti-fibrotic treatment in a rodent model of acute lung injury induced by sulfur dioxide

Cited by 12 publications

References 43 publications

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

Edible bird's nest inhibits the inflammation and regulates the immunological balance of lung injury mice by SO2

Prevention of tracheal stenosis with pirfenidone after tracheotomy: An experimental study

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Edible bird's nest inhibits the inflammation and regulates the immunological balance of lung injury mice by SO₂