Oxidative Stress in Experimental Models of Acute Lung Injury

Mokrá, Daniela; Mokrý, Juraj

doi:10.1007/978-981-32-9366-3_2

Cited by 5 publications

(3 citation statements)

References 208 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, Dex+los group showed significant increasing in levels of NO and SOD, and decreasing levels of MDA, MMP-9, ICAM-1 and NF-kB expression. 49 –51 Moreover, the proliferation of human lung fibroblasts and induction of alveolar epithelial cell apoptosis were apparently increased by the binding of angiotensin II to the AT1 receptor. Losartan prevents fibrosis mainly via inhibition of binding of angiotensin II to the AT1 receptor.…”

Section: Disscussionmentioning

confidence: 99%

Dexamethasone and losartan combination treatment protected cigarette smoke-induced COPD in rats

2020

View full text Add to dashboard Cite

Chronic Obstructive Pulmonary Disease (COPD) is a dangerous prevalent smoking-related disease characterized by abnormal inflammation and oxidative stress and expected to be the third cause of death in the world next decade. Corticosteroids have low effects in decreasing numbers of inflammatory mediators specifically in long-term use. Our study designed to investigate the possible protective effects of combined dexamethasone (Dex) (2mg/kg) and losartan (Los) (30mg/kg angiotensin receptor blocker, it possesses antioxidant and anti-inflammatory properties in lung injury in mice) against cigarette -smoke (CS) induced COPD in rats compared with dexamethasone and losartan. Male Sprague Dawley rats (N = 40) divided into five groups (n = 8): control group, CS group, Dex group, Los group, and Dex +Los group. COPD induced in rats by CS exposure twice daily for 10 weeks. After the specified treatment period, bronchoalveolar lavage fluid (BALF) and lung tissue were collected for measurement of SOD, NO, MDA, ICAM-, MMP-9, CRP, NF-κB and histopathology scoring. Our results indicated that Los+Dex significantly prevent CS-induced COPD emphysema, congested alveoli, and elevation of lung injury parameters in BALF. They also showed a significant decrease in MDA, ICAM-1, MMP-9, CRP, and NF-κB and a significant increase in SOD and NO. In conclusion, adding Los to Dex potentiating their activity in inhibition the progression of COPD based on its activity on oxidative stress, inflammation, and NF-κB protein expression.

show abstract

Section: Disscussionmentioning

confidence: 99%

Dexamethasone and losartan combination treatment protected cigarette smoke-induced COPD in rats

2020

View full text Add to dashboard Cite

show abstract

“…The crystal structure of TGF‐β1 with a resolution of 3.0 Å (PDB Id: 3KFD) was selected for in silico molecular docking study with Curcumin. The molecular docking was performed in AutoDock 4.2 27,28 . Chain A from the ternary complex of TGF‐β1 was extracted and considered as the macromolecule.…”

Section: Methodsmentioning

confidence: 99%

The unique molecular targets associated antioxidant and antifibrotic activity of curcumin in in vitro model of acute lung injury: A proteomic approach

et al. 2021

View full text Add to dashboard Cite

Bleomycin (BLM) injury is associated with the severity of acute lung injury (ALI) leading to fibrosis, a high‐morbidity, and high‐mortality respiratory disease of unknown etiology. BLM‐induced ALI is marked by the activation of a potent fibrogenic cytokine transcription growth factor beta‐1 (TGFβ‐1), which is considered a critical cytokine in the progression of alveolar injury. Previously, our work demonstrated that a diet‐derived compound curcumin (diferuloylmethane), represents its antioxidative and antifibrotic application in TGF‐β1‐mediated BLM‐induced alveolar basal epithelial cells. However, curcumin‐specific protein targets, as well as its mechanism using mass spectrometry‐based proteomic approach, remain elusive. To elucidate the underlying mechanism, a quantitative proteomics approach and bioinformatics analysis were employed to identify the protein targets of curcumin in BLM or TGF‐β1‐treated cells. With subsequent in vitro experiments, curcumin‐related pathways and cellular processes were predicted and validated. The current study discusses two separate proteomics experiments using BLM and TGF‐β1‐treated cells with the proteomics approach, various unique target proteins were identified, and proteomic analysis revealed that curcumin reversed the expressions of unique proteins like DNA topoisomerase 2‐alpha (TOP2A), kinesin‐like protein (KIF11), centromere protein F (CENPF), and so on BLM or TGF‐β1 injury. For the first time, the current study reveals that curcumin restores TGF‐β1 induced peroxisomes like PEX‐13, PEX‐14, PEX‐19, and ACOX1. This was verified by subsequent in vitro assays. This study generated molecular evidence to deepen our understanding of the therapeutic role of curcumin at the proteomic level and may be useful to identify molecular targets for future drug discovery.

show abstract

“…Oxidative stress in lung tissue, whether originating from an overproduction of reactive oxygen species or malfunction of the antioxidant system, contributes significantly to the pathophysiology of ARDS (Mokra & Mokry, 2020). However, there are contradictory results about the relationship between exercise and oxidative stress.…”

mentioning

confidence: 99%

Effects of aerobic exercise on lipopolysaccharide‐induced experimental acute lung injury in the animal model of type 1 diabetes mellitus

Ömercioğlu

Akat

Ficicilar

et al. 2021

Experimental Physiology

View full text Add to dashboard Cite

Acute lung injury (ALI) is a life-threatening respiratory condition. Diabetes (DM) is a metabolic disease characterized by hyperglycaemia. There is an ongoing debate concerning whether there is a protective effect of diabetes in ALI. Exercise is a special type of physical activity that has numerous beneficial effects. The aim of our study was to investigate the effects of diabetes and exercise on the prognosis of ALI. Male Wistar albino rats were divided into two groups (sedentary and exercise). Both groups were divided into four subgroups: Control, ALI, DM, DM+ALI (n = 6 each). Diabetes was induced by injection of streptozotocin (50 mg/kg i.p.). The maximal exercise capacity was determined with the incremental load test. Animals were exercised on a treadmill for 45 min at 70% of maximal exercise capacity, 5 days a week for 12 weeks. Acute lung injury was induced by intratracheal injection of lipopolysaccharide (100 μg/100 g body weight) 24 h before the end of the experiment. We performed arterial blood gas analysis. Redox status was measured in both plasma and lung tissue. Malondialdehyde and 8-hydroxy-2′-deoxyguanosine levels were measured in lung tissue. Lung tissue was evaluated histologically. Acute lung injury caused significant damage in the lung tissue, which was verified histologically, with an increase in oxidative stress parameters.Exercise prevented the lung damage induced by ALI and reduced oxidative stress in the lung tissue. Diabetes did not alter the magnitude of damage done by ALI.Exercise showed a protective effect against DM and ALI in rats. The effect of DM was insignificant for the prognosis of ALI.

show abstract

Oxidative Stress in Experimental Models of Acute Lung Injury

Cited by 5 publications

References 208 publications

Dexamethasone and losartan combination treatment protected cigarette smoke-induced COPD in rats

Dexamethasone and losartan combination treatment protected cigarette smoke-induced COPD in rats

The unique molecular targets associated antioxidant and antifibrotic activity of curcumin in in vitro model of acute lung injury: A proteomic approach

Effects of aerobic exercise on lipopolysaccharide‐induced experimental acute lung injury in the animal model of type 1 diabetes mellitus

Contact Info

Product

Resources

About