Oxidative Stress Response of PM2.5 and Mixed Toxic Gases to Rat Trachea and Lung Tissue

Author(s):  
Shouqin Wang ◽  
Jia Xu ◽  
Biao Yang ◽  
Dongmei Chen ◽  
Hui Zhao ◽  
...  

Abstract Background:We performed this study to explore the inflammation and oxidative stress responses of rat trachea and lung caused by PM2.5 and mixed toxic gas.Materials and methods:Eighty-four Wistar rats were randomly assigned to receive exposure to PM2.5 and toxic gases containing carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2) or saline. Microflora in rat respiratory tract were investigated through testing secretion taken from posterior pharyngeal wall on Day 1, 7 and 30. Trachea and lung tissues were processed for scanning electron microscopic (SEM) and transmission electron microscopic (TEM) examinations. Cytokines in rat bronchoalveolar lavage fluid (BALF), serum and lung tissues were analyzed via enzyme-linked immunosorbent assay and real-time quantitative PCR.Results:Eight aerobes and seven anaerobes were firstly detected after exposure (p<0.01, respectively). Most of them are the pathogenic bacteria or opportunistic pathogen. SEM and TEM observations suggested that both normal structure of trachea and lung tissue were injured after exposure to PM2.5 with mixed toxic gas and the injure degree was concentration- and time-dependent. Interleukin 4 (IL-4), interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) expression in the BALF and lung tissue markedly increased on Day 1 and 7 (p<0.01, respectively). Interferon γ (IFN-γ) did not show significant change after exposure. On Day 30, all the detected cytokines decreased and even disappeared. All detected cytokines in the serum had no significant difference before and after exposure (p>0.05, respectively).Conclusion:PM2.5 with mixed toxic gas can lead to dysbacteriosis in respiratory tract and destroy the normal structure of trachea and lung tissue. The injure degree was concentration- and time-dependent. Local inflammatory response instead of systemic reaction may be predominant in the response of rat respiratory tract to PM2.5 with mixed toxic gas.

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jiahuan Tong ◽  
Zhisong Wu ◽  
Yuchen Wang ◽  
Qingxun Hao ◽  
Haoge Liu ◽  
...  

Objective. The study aims to research the interventional effect and mechanism of astragaloside IV (Ast) synergizing with ferulic acid (FA) on idiopathic pulmonary fibrosis (IPF) induced by bleomycin in mice. Methods. The mice were randomly divided into seven groups with 10 mice in each group, namely, a sham operation group, a model group, a miRNA-29b (miR-29) group, a miR-29b negative control group (NC group), a FA group, an Ast group, and a combination group. A mouse model of pulmonary fibrosis was established by intratracheal instillation of bleomycin. Samples were collected after 28 days of continuous administration. Hematoxylin and eosin (HE) and Masson staining were used to observe pathological changes in the lung tissue, and the degree of fibrosis was evaluated using the hydroxyproline content. Changes in transforming growth factor-β1 (TGF-β1) and Smad3 in the lung were observed using immunohistochemistry. Enzyme-linked immunosorbent assay (ELISA) was used to detect the level of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) in the serum. PCR was used to detect the expression of the miR-29b, TGF-β1, Smad3, and nuclear factor E2-related factor 2 (Nrf2) genes. Western blotting was used to detect the content of the TGF-β/Smad3 protein. Results. Ferulic acid combined with astragaloside IV reduced the degree of pulmonary fibrosis and the synthesis of hydroxyproline in lung tissue. The combination of the two also regulated the oxidative stress response , TGF-β1/Smad3 pathway and miR-29b in lung tissue. Conclusion. Astragaloside IV combined with ferulic acid regulated the oxidative stress of lung tissues and TGF-β1/Smad3 signaling through miR-29b, thereby reducing the degree of pulmonary fibrosis. This provides a reference direction for the clinical treatment of IPF patients.


1998 ◽  
Vol 274 (3) ◽  
pp. L396-L403 ◽  
Author(s):  
Andrew J. Ghio ◽  
Jacqueline D. Carter ◽  
Judy H. Richards ◽  
Luisa E. Brighton ◽  
John C. Lay ◽  
...  

The atmosphere constitutes a prime vehicle for the movement and redistribution of metals. Metal exposure can be associated with an oxidative stress. We tested the hypothesis that, in response to an iron-containing particle, the human respiratory tract will demonstrate an increased expression of both lactoferrin and ferritin as the host attempts to transport and store the metal in a chemically less-reactive form and therefore diminish the oxidative stress the particle presents. Subjects ( n = 22) were instilled with 20 ml of saline and 20 ml of an iron-containing particle suspended in saline in a right middle lobe bronchus and a lingular bronchus, respectively. At either 1, 2, or 4 days after this exposure, the volunteer was lavaged for a sample of the lower respiratory tract, and concentrations ofl-ferritin, transferrin, and lactoferrin were measured by enzyme immunoassay, immunoprecipitin analysis, and enzyme-linked immunosorbent assay (ELISA), respectively. Transferrin receptor was also quantified by ELISA. The concentrations of l-ferritin in the lavage fluid of lung exposed to particles were significantly increased relative to the levels of the protein in the segment exposed to saline. Relative to saline instillation, transferrin was significantly diminished after exposure to the iron-containing particle, whereas both lactoferrin and transferrin receptor concentrations in the segment of the lung exposed to the particle were significantly elevated. We conclude that instillation of an iron-containing particle was associated with a disequilibrium in iron metabolism in the lower respiratory tract. The response included increased ferritin and lactoferrin concentrations, whereas transferrin concentrations diminished. This coordinated series of reactions by the host effects a decrease in the availability of catalytically reactive iron to likely diminish the consequent oxidative stress to the human host.


2020 ◽  
Vol 19 (7) ◽  
pp. 1429-1433
Author(s):  
Jihong Shu ◽  
Zhenjiao Fang ◽  
Xinjun Xiong

Purpose: To investigate the effect of penehyclidine hydrochloride (PHC) on interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), hypoxia inducible factor-1α (HIF-1α), and oxidative stress levels in lung tissues of acute lung injury (ALI) neonatal rats.Methods: 40 male Sprague-Dawley (SD) rats were assigned to model, low-dose PHC, high-dose PHC, and control groups (n = 10). Levels of IL-6, TNF-α and HIF-1α were evaluated by enzyme-linked immunosorbent assay (ELISA). Pulmonary lesions were determined histologically using H&E staining.Results: The lung tissue levels of IL-6, TNF-α and HIF-1α were significantly higher in model rats than in control rats, and significantly lower in PHC-treated rats than in model group, with decrease in levels as PHC dose increased (p < 0.05). The lung tissue activity of MPO and level of MDA in model rats were significantly higher than those in control rats, but significantly lower in the lung tissues of the two PHC groups than in the model group; decrease in levels occurred as PHC dose increased (p < 0.05).Conclusion: PHC decreases the lung and serum levels of IL-6, TNF-α and HIF-1α in a rat model of ALI, and mitigates pulmonary oxidative stress and lung tissue damage. Thus, penehyclidine hydrochloride may be useful to mitigate ALI-induced damage in patients. However, further studies and clinical trials are required to ascertain this Keywords: Penehyclidine hydrochloride, Alveolar septum, Acute lung injury, Inflammatory cells, IL-6, TNF-α, HIF-1α, Oxidative stress


2020 ◽  
Vol 9 (1) ◽  
pp. 35-42
Author(s):  
Yu. A. Kirillov ◽  
I. A. Chernov ◽  
E. M. Malysheva ◽  
S. E. Timofeev ◽  
V. I. Kukushkin ◽  
...  

Radiation exposure to the chest organs used in the complex treatment of neoplasms is often accompanied by the development of radiation pneumonitis, fibrosis and respiratory failure.The aim of the study was to evaluate oxidative stress and endothelial dysfunction in radio-induced lung damage and possibility of their correction with a pulmonary surfactant preparation.Material and methods. Lung tissue samples of 82 male Wistar rats were investigated in the study. Single local irradiation of animals was performed with the X-ray RUM-17 unit at a dose 12 Gy. The quantitative content and fractional composition of phospholipids of pulmonary surfactant were determined in the study. Oxidative stress was detected using Raman spectroscopy, endothelial dysfunction was detected immunohistochemically.Results. Oxidative stress and endothelial dysfunction were registered starting from the first day of the experiment, and manifested by an increased content of free radicals and a decrease in endothelial function indices supported by precise spectroscopic, immunohistochemical and electron microscopic methods. With application of Surfactant-BL preparation oxidative stress manifestations were eliminated to the beginning of the intermediate stage of the experiment, and were preserved without correction until its completion.Conclusions. Three-fold intratracheal administration of a pulmonary surfactant preparation implements an antioxidant, immunomodulatory and compensating effect attenuating the alterative effect of oxidative stress and its initiating impact on the development of endothelial dysfunction. Native surfactant having a pronounced effect on all components of the lung tissue including alveolocytes of the first and second types and endothelial cells of the capillaries of the lung results in the correction of endothelial dysfunction.


2012 ◽  
Vol 40 (3) ◽  
pp. 943-953 ◽  
Author(s):  
H Zhang ◽  
J-W Wang ◽  
Y Xu ◽  
K Zhang ◽  
B Yi ◽  
...  

OBJECTIVE: To investigate the effects of β-(3,4-dihydroxyphenyl)lactic acid on oxidative stress stimulated by high glucose levels in human peritoneal mesothelial cells (HPMCs) in vitro. METHODS: HPMCs were incubated with 100 mol/l glucose followed by 0.625 – 20 mg/ml β-(3,4-dihydroxyphenyl)lactic acid. Reactive oxygen species (ROS) were quantified by flow cytometry. Relative levels of fibronectin-1 (FN1), collagen-I α1 (COL1A1), endothelin-1 (EDN1) and haem oxygenase-1 (HMOX1) mRNA and protein were quantified by real-time reverse transcription—polymerase chain reaction and Western blotting, respectively. Absolute levels of FN1 and COLIA1 were quantified by enzyme-linked immunosorbent assay. RESULTS: β-(3,4-Dihydroxyphenyl)lactic acid significantly decreased ROS levels, and EDN1 mRNA and protein levels, in dose- and time-dependent manners. HMOX1 mRNA and protein levels were significantly increased by β-(3,4-dihydroxyphenyl)lactic acid in dose-dependent manners. COL1A1 and FN1 mRNA and protein levels were significantly decreased by β-(3,4-dihydroxyphenyl)lactic acid in dose- and time-dependent manners. CONCLUSIONS: β-(3,4-Dihydroxyphenyl)lactic acid inhibited oxidative stress and reversed increases in FN1 and COLIA1 induced by high glucose levels in HPMCs. This may contribute to a protective role in peritoneal fibrosis.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Jie Yun ◽  
Jinyu Ren ◽  
Yufei Liu ◽  
Lijuan Dai ◽  
Liqun Song ◽  
...  

Abstract Background Circular RNAs (circRNAs) have been considered as pivotal biomarkers in Diabetic nephropathy (DN). CircRNA ARP2 actin-related protein 2 homolog (circ-ACTR2) could promote the HG-induced cell injury in DN. However, how circ-ACTR2 acts in DN is still unclear. This study aimed to explore the molecular mechanism of circ-ACTR2 in DN progression, intending to provide support for the diagnostic and therapeutic potentials of circ-ACTR2 in DN. Methods RNA expression analysis was conducted by the quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell growth was measured via Cell Counting Kit-8 and EdU assays. Inflammatory response was assessed by Enzyme-linked immunosorbent assay. The protein detection was performed via western blot. Oxidative stress was evaluated by the commercial kits. The molecular interaction was affirmed through dual-luciferase reporter and RNA immunoprecipitation assays. Results Circ-ACTR2 level was upregulated in DN samples and high glucose (HG)-treated human renal mesangial cells (HRMCs). Silencing the circ-ACTR2 expression partly abolished the HG-induced cell proliferation, inflammation and extracellular matrix accumulation and oxidative stress in HRMCs. Circ-ACTR2 was confirmed as a sponge for miR-205-5p. Circ-ACTR2 regulated the effects of HG on HRMCs by targeting miR-205-5p. MiR-205-5p directly targeted high-mobility group AT-hook 2 (HMGA2), and HMGA2 downregulation also protected against cell injury in HG-treated HRMCs. HG-mediated cell dysfunction was repressed by miR-205-5p/HMGA2 axis. Moreover, circ-ACTR2 increased the expression of HMGA2 through the sponge effect on miR-205-5p in HG-treated HRMCs. Conclusion All data have manifested that circ-ACTR2 contributed to the HG-induced DN progression in HRMCs by the mediation of miR-205-5p/HMGA2 axis.


Healthcare ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 368
Author(s):  
Rosamaria Militello ◽  
Simone Luti ◽  
Matteo Parri ◽  
Riccardo Marzocchini ◽  
Riccardo Soldaini ◽  
...  

Background: Most studies on oxidative stress markers and antioxidant levels have been conducted in male athletes, although female participation in sport has increased rapidly in the past few decades. In particular, it could be important to assess oxidative stress markers in relation to the training load because the anaerobic path becomes predominant in high-intensity actions. Methods: Ten female professional basketball players, performing five 2 h-lasting training sessions per week, and 10 sedentary control women were investigated. Capillary blood and saliva samples were collected in the morning before the training session. The antioxidant capacity and the levels of reactive oxygen metabolites on plasma were determined measuring Reactive Oxygen Metabolite and Biological Antioxidant Potential (d-ROMs and the BAP Test). Salivary cortisol was detected by using commercial enzyme-linked immunosorbent assay kit. Results: The antioxidant capacity (BAP value) was significantly higher in elite basketball players (21.2%; p < 0.05). Conversely, cortisol (51%; p < 0.009) and the levels of oxidative species (d-ROM, 21.9%; p < 0.05) showed a significant decrease in elite athletes.


Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P&lt;0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.


2016 ◽  
Vol 33 (2) ◽  
pp. 171-181 ◽  
Author(s):  
Bing Xia ◽  
Kangcheng Chen ◽  
Yingnan Lv ◽  
Damin Huang ◽  
Jing Liu ◽  
...  

Objectives: Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic derivative of manganese (Mn) and is used as an antiknock agent and octane enhancer in gasoline. In this article, we tested the oxidative stress and heat stress protein (Hsp) 70 levels of gasoline station attendants to explore potential plasma biomarkers. Furthermore, the dose–response relationship was also identified. Methods: A total of 144 workers, including 96 petrol fillers and 48 cashiers, participated in the study. Ambient concentrations of benzene, toluene, ethylbenzene, and xylene (BTEX) and Mn were monitored at nine filling stations. During the measuring process, the individual cumulative exposure index was calculated. Plasma oxidative stress and Hsp70 levels were also analysed using enzyme-linked immunosorbent assay. Results: The BTEX time-weighted average in office areas was significantly lower than in refuelling areas ( p < 0.05). In refuelling areas, the content of Mn ranged from 6.44 μg/m3 to 127.34 μg/m3, which was much higher than that in office areas (3.16–7.22 μg/m3; p < 0.05). Exposed workers had significantly different plasma oxidative stress indicators compared with the control group, respectively: superoxide dismutase (SOD), 39.18 ± 6.05 U/mL versus 52.84 ± 3.87 U/mL; glutathione peroxidase (GSH-Px), 186.07 ± 15.63 U versus 194.38 ± 10.42 U; and malondialdehyde (MDA), 1.68 ± 0.52 nmol/L versus 1.43 ± 0.64 nmol/L (in all comparisons, p < 0.05). Plasma Hsp70 level in the exposed group (2.77 ± 0.64 ng/mL) was significantly higher than in the control group (2.32 ± 0.87 ng/mL; p < 0.05). Furthermore, Hsp70 levels were inversely correlated with the activities of SOD ( r = −0.305) and GSH-Px ( r = −0.302) in the exposed group ( p < 0.05). Moreover, a positive correlation ( r = 0.653) was found between plasma Hsp70 levels and plasma MDA levels ( p < 0.05). Conclusion: Exposure to MMT-containing gasoline may result in increasing reactive oxygen stress among filling station attendants. Plasma Hsp70 levels could be used as a sensitive responsive biomarker for exposed workers.


2010 ◽  
Vol 3 (6) ◽  
pp. 414-420 ◽  
Author(s):  
Subir Kumar Das ◽  
Sukhes Mukherjee

Background: Alcohol abuse is a systemic disorder. The deleterious health effects of alcohol consumption may result in irreversible organ damage. By contrast, there currently is little evidence for the toxicity of chronic alcohol use on lung tissue. Hence, in this study we investigated long-term effects of ethanol in the lung.Results: Though body weight of rats increased significantly with duration of exposure compared to its initial weight, there was no significant change in relative weight (g/100 g body weight) of lung due to ethanol exposure. The levels of thiobarbituric acid reactive substances (TBARS), nitrite, protein carbonyl, oxidized glutathione (GSS G), redox ratio (GSS G/ GSH ) and GST activity elevated; while reduced glutathione (GSH ) level and activities of glutathione reductase (GR), glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD) and Na+K+ATPase reduced significantly with duration of ethanol exposure in the lung homogenate compared to the control group. Total matrix metalloproteinase activity elevated in the lung homogenate with time of ethanol consumption. Histopathologic examination also demonstrated that severity of lung injury enhanced with duration of ethanol exposure.Methods: 16–18 week-old male albino Wistar strain rats weighing 200–220 g were fed with ethanol (1.6 g/kg body weight/day) up to 36 weeks. At the end of the experimental period, blood samples were collected from reteroorbital plexus to determine blood alcohol concentration and the animals were sacrificed. Various oxidative stress-related biochemical parameters, total matrix metalloproteinase activity and histopathologic examinations of the lung tissues were performed.Conclusions: Results of this study indicate that long-term ethanol administration aggravates systemic and local oxidative stress, which may be associated with lung tissue injury.


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