scholarly journals Methylene Blue Attenuates Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Liangrong Wang ◽  
Baihui Chen ◽  
Bi Lin ◽  
Yuzhu Ye ◽  
Caiying Bao ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Lung Injury ◽  
Lung Tissue ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Lavage Fluid ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Sprague Dawley Rats ◽  
Healthy Adult Male

Objective. This study was aimed to investigate the protective effect of methylene blue against lung injury induced by reperfusion of ischemic hindlimb in a rat model. Methods. Twenty-four healthy adult male Sprague-Dawley rats were equally randomized into three groups: sham (SM) group, ischemia reperfusion (IR) group, and methylene blue (MB) group. Rats in both IR and MB groups were subjected to 4 h of ischemia by clamping the left femoral artery and then followed by 4 h of reperfusion. Treatment with 1% methylene blue (50 mg/kg) was administrated intraperitoneally at 10 min prior to reperfusion in the MB group. After 4 h of reperfusion, malondialdehyde (MDA) level, myeloperoxidase (MPO), and superoxide dismutase (SOD) activities in lung tissue were detected; inflammatory cytokines, including IL-1β and IL-6, were measured in bronchoalveolar lavage fluid (BALF); correspondingly, the morphological changes and water content in both gastrocnemius muscle and lung samples were evaluated. Results. Hindlimb IR caused remarkable morphological abnormalities and edema in both muscle and lung tissues. SOD activity was decreased, both the MPO activity and MDA level in lung tissue, as well as IL-1β and IL-6 levels in BALF, were increased in the IR group (p<0.05). Compared with the IR group, SOD activity was increased, whereas MPO activity and MDA level in lung tissue and IL-1β and IL-6 levels in BALF were decreased in the MB group (p<0.05). Also, the histological damage and edema in both lung and muscle tissues were significantly attenuated by the treatment of methylene blue. Conclusion. Methylene blue attenuates lung injury induced by hindlimb IR in rats, at least in part, by inhibiting oxidative stress.

scholarly journals Anti-Inflammatory and Anticoagulative Effects of Paeonol on LPS-Induced Acute Lung Injury in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Pin-Kuei Fu ◽  
Chieh-Liang Wu ◽  
Tung-Hu Tsai ◽  
Ching-Liang Hsieh
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Lavage Fluid ◽  
Polymorphonuclear Neutrophils ◽  
Sprague Dawley ◽  
Intratracheal Administration ◽  
Sprague Dawley Rats ◽  
Anti Inflammatory

Paeonol is an active component of Moutan Cortex Radicis and is widely used as an analgesic, antipyretic, and anti-inflammatory agent in traditional Chinese medicine. We wanted to determine the role of paeonol in treating adult respiratory distress syndrome (ARDS). We established an acute lung injury (ALI) model in Sprague-Dawley rats, which was similar to ARDS in humans, using intratracheal administration of lipopolysaccharide (LPS). The intraperitoneal administration of paeonol successfully reduced histopathological scores and attenuated myeloperoxidase-reactive cells as an index of polymorphonuclear neutrophils infiltration and also reduces inducible nitric oxide synthase expression in the lung tissue, at 16 h after LPS administration. In addition, paeonol reduced proinflammatory cytokines in bronchoalveolar lavage fluid, including tumor-necrosis factor-α, interleukin-1β, interleukin-6, and plasminogen-activated inhibition factor-1. These results indicated that paeonol successfully attenuates inflammatory and coagulation reactions to protect against ALI.

scholarly journals Does methylene blue attenuate inflammation in nonischemic lungs after lung transplantation?

2018 ◽  
Vol 44 (5) ◽  
pp. 378-382
Author(s):  
Marcus da Matta Abreu ◽  
Francine Maria de Almeida ◽  
Kelli Borges dos Santos ◽  
Emílio Augusto Campos Pereira de Assis ◽  
Rafael Kenji Fonseca Hamada ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Lung Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Lung Parenchyma ◽  
Saline Group ◽  
Intercellular Adhesion Molecule ◽  
Sprague Dawley ◽  
Intercellular Adhesion Molecule 1 ◽  
Sprague Dawley Rats

ABSTRACT Objective: To evaluate whether methylene blue (MB) could minimize the effects of ischemia-reperfusion injury in the nonischemic lung on a lung transplantation rodent model. Methods: Forty female Sprague-Dawley rats were divided into 20 donors and 20 recipients. The 20 recipient rats were divided into two groups (n = 10) according to the treatment (0.9% saline vs. 1% MB solutions). All animals underwent unilateral lung transplantation. Recipients received 2 mL of saline or MB intraperitoneally prior to transplantation. After 2 h of reperfusion, the animals were euthanized and histopathological and immunohistochemical analyses were performed in the nonischemic lung. Results: There was a significant decrease in inflammation-neutrophil count and intercellular adhesion molecule-1 (ICAM-1) expression in lung parenchyma were higher in the saline group in comparison with the MB group-and in apoptosis-caspase-3 expression was higher in the saline group and Bcl-2 expression was higher in MB group. Conclusions: MB is an effective drug for the protection of nonischemic lungs against inflammation and apoptosis following unilateral lung transplantation in rats.

scholarly journals Necrostatin-1 Synergizes the Pan Caspase Inhibitor to Attenuate Lung Injury Induced by Ischemia Reperfusion in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Liangrong Wang ◽  
Baihui Chen ◽  
Xiangqing Xiong ◽  
Shunli Chen ◽  
Lida Jin ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lung Tissue ◽  
Inflammatory Markers ◽  
Bronchoalveolar Lavage Fluid ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Lung ◽  
Lavage Fluid ◽  
Caspase Inhibitor ◽  
Interacting Protein

Background. Both apoptosis and necroptosis have been recognized to be involved in ischemia reperfusion-induced lung injury. We aimed to compare the efficacies of therapies targeting necroptosis and apoptosis and to determine if there is a synergistic effect between the two therapies in reducing lung ischemia reperfusion injury. Methods. Forty Sprague-Dawley rats were randomized into 5 groups: sham (SM) group, ischemia reperfusion (IR) group, necrostatin-1+ischemia reperfusion (NI) group, carbobenzoxy-Val-Ala-Asp-fluoromethylketone+ischemia reperfusion (ZI) group, and necrostatin-1+carbobenzoxy-Val-Ala-Asp-fluoromethylketone+ischemia reperfusion (NZ) group. The left lung hilum was exposed without being clamped in rats from the SM group, whereas the rats were subjected to lung ischemia reperfusion by clamping the left lung hilum for 1 hour, followed by reperfusion for 3 hours in the IR group. 1 mg/kg necrostatin-1 (Nec-1: a specific necroptosis inhibitor) and 3 mg/kg carbobenzoxy-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk: a pan caspase inhibitor) were intraperitoneally administrated prior to ischemia in NI and ZI groups, respectively, and the rats received combined administration of Nec-1 and z-VAD-fmk in the NZ group. Upon reperfusion, expressions of receptor-interacting protein 1 (RIP1), receptor-interacting protein 3 (RIP3), and caspase-8 were measured, and the flow cytometry analysis was used to assess the cell death patterns in the lung tissue. Moreover, inflammatory marker levels in the bronchoalveolar lavage fluid and pulmonary edema were evaluated. Results. Both Nec-1 and z-VAD-fmk, either alone or in combination, significantly reduced morphological damage, inflammatory markers, and edema in lung tissues following reperfusion, and cotreatment of z-VAD-fmk with Nec-1 produced the optimal effect. The rats treated with Nec-1 had lower levels of inflammatory markers in the bronchoalveolar lavage fluid than those receiving z-VAD-fmk alone ( P < 0.05 ). Interestingly, the z-VAD-fmk administration upregulated RIP1 and RIP3 expressions in the lung tissue from the ZI group compared to those in the IR group ( P < 0.05 ). Reperfusion significantly increased the percentages of necrotic and apoptotic cells in lung tissue single-cell suspension, which could be decreased by Nec-1 and z-VAD-fmk, respectively ( P < 0.05 ). Conclusions. Nec-1 synergizes the pan caspase inhibitor to attenuate lung ischemia reperfusion injury in rats. Our data support the potential use of Nec-1 in lung transplantation-related disorders.

scholarly journals Remote Inflammatory Preconditioning Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Intrinsic Apoptosis in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yong Liu ◽  
Jiahang Xu ◽  
Liang Zhao ◽  
Jing Cheng ◽  
Baojun Chen
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Animal Experiments ◽  
Intrinsic Apoptosis ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Lung Protection ◽  
Sprague Dawley Rats ◽  
The Right

Background. Acute lung injury (ALI) always leads to severe inflammation. As inflammation and oxidative stress are the common pathological basis of endotoxin-induced inflammatory injury and ischemic reperfusion injury (IRI), we speculate that remote ischemic preconditioning (RIPC) can be protective for ALI when used as remote inflammatory preconditioning (RInPC). Method. A total of 21 Sprague-Dawley rats were used for the animal experiments. Eighteen rats were equally and randomly divided into the control (NS injection), LPS (LPS injection), and RInPC groups. The RInPC was performed prior to the LPS injection via tourniquet blockage of blood flow to the right hind limb and adopted three cycles of 5 min tying followed by 5 min untying. Animals were sacrificed 24 hours later. There were 2 rats in the LPS group and 1 in the RInPC group who died before the end of the experiment. Supplementary experiments in the LPS and RInPC groups were conducted to ensure that 6 animals in each group reached the end of the experiment. Results. In the present study, we demonstrated that the RInPC significantly attenuated the LPS-induced ALI in rats. Apoptotic cells were reduced significantly by the RInPC, with the simultaneous improvement of apoptosis-related proteins. Reduction of MPO and MDA and increasing of SOD activity were found significantly improved by the RInPC. Increasing of TNF-α, IL-1β, and IL-6 induced by the LPS was inhibited, while IL-10 was significantly increased by RInPC, compared to the LPS group. Conclusion. RInPC could inhibit inflammation and attenuate oxidative stress, thereby reducing intrinsic apoptosis and providing lung protection in the LPS-induced ALI in rats.

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

2020 ◽  
pp. 096032712095001
Author(s):  
Samia S Sokar ◽  
Esraa H Afify ◽  
Enass Y Osman
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Lavage Fluid ◽  
Control Group ◽  
Chronic Obstructive ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Obstructive Pulmonary Disease ◽  
Sprague Dawley Rats

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.

scholarly journals Arachidonic acid in postshock mesenteric lymph induces pulmonary synthesis of leukotriene B4

2008 ◽  
Vol 104 (4) ◽  
pp. 1161-1166 ◽  
Author(s):  
Janeen R. Jordan ◽  
Ernest E. Moore ◽  
Eric L. Sarin ◽  
Sagar S. Damle ◽  
Sara B. Kashuk ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Sprague Dawley ◽  
Bioactive Lipids ◽  
Mesenteric Lymph ◽  
Sprague Dawley Rats

Mesenteric lymph is the mechanistic link between splanchnic hypoperfusion and acute lung injury (ALI), but the culprit mediator(s) remains elusive. Previous work has shown that administration of a phospholipase A2(PLA2) inhibitor attenuated postshock ALI and also identified a non-ionic lipid within the postshock mesenteric lymph (PSML) responsible for polymorphonuclear neutrophil (PMN) priming. Consequently, we hypothesized that gut-derived leukotriene B4(LTB4) is a key mediator in the pathogenesis of ALI. Trauma/hemorrhagic shock (T/HS) was induced in male Sprague-Dawley rats and the mesenteric duct cannulated for lymph collection/diversion. PSML, arachidonic acid (AA), and a LTB4receptor antagonist were added to PMNs in vitro. LC/MS/MS was employed to identify bioactive lipids in PSML and the lungs. T/HS increased AA in PSML and increased LTB4and PMNs in the lung. Lymph diversion decreased lung LTB4by 75% and PMNs by 40%. PSML stimulated PMN priming (11.56 ± 1.25 vs. 3.95 ± 0.29 nmol O2−/min; 3.75 × 105cells/ml; P < 0.01) that was attenuated by LTB4receptor blockade (2.64 ± 0.58; P < 0.01). AA stimulated PMNs to produce LTB4, and AA-induced PMN priming was attenuated by LTB4receptor antagonism. Collectively, these data indicate that splanchnic ischemia/reperfusion activates gut PLA2-mediated release of AA into the lymph where it is delivered to the lungs, provoking LTB4production and subsequent PMN-mediated lung injury.

scholarly journals Caffeine Mitigates Lung Inflammation Induced by Ischemia-Reperfusion of Lower Limbs in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Wei-Chi Chou ◽  
Ming-Chang Kao ◽  
Chung-Tai Yue ◽  
Pei-Shan Tsai ◽  
Chun-Jen Huang
Keyword(s):  
Lung Inflammation ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Lavage Fluid ◽  
Lower Limbs ◽  
Sham Operation ◽  
Myeloperoxidase Activity ◽  
Sprague Dawley ◽  
Inflammatory Protein ◽  
Sprague Dawley Rats

Reperfusion of ischemic limbs can induce inflammation and subsequently cause acute lung injury. Caffeine, a widely used psychostimulant, possesses potent anti-inflammatory capacity. We elucidated whether caffeine can mitigate lung inflammation caused by ischemia-reperfusion (IR) of the lower limbs. Adult male Sprague-Dawley rats were randomly allocated to receive IR, IR plus caffeine (IR + Caf group), sham-operation (Sham), or sham plus caffeine (n=12in each group). To induce IR, lower limbs were bilaterally tied by rubber bands high around each thigh for 3 hours followed by reperfusion for 3 hours. Caffeine (50 mg/kg, intraperitoneal injection) was administered immediately after reperfusion. Our histological assay data revealed characteristics of severe lung inflammation in the IR group and mild to moderate characteristic of lung inflammation in the IR + Caf group. Total cells number and protein concentration in bronchoalveolar lavage fluid of the IR group were significantly higher than those of the IR + Caf group (P<0.001andP=0.008, resp.). Similarly, pulmonary concentrations of inflammatory mediators (tumor necrosis factor-α, interleukin-1β, and macrophage inflammatory protein-2) and pulmonary myeloperoxidase activity of the IR group were significantly higher than those of the IR + Caf group (allP<0.05). These data clearly demonstrate that caffeine could mitigate lung inflammation induced by ischemia-reperfusion of the lower limbs.

Ischemia-reperfusion lung injury attenuated by ATP-MgCl2 in rats

1994 ◽  
Vol 76 (2) ◽  
pp. 545-552 ◽  
Author(s):  
K. Hsu ◽  
D. Wang ◽  
S. Y. Wu ◽  
C. Y. Shen ◽  
H. I. Chen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Degradation Product ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Kidney Liver ◽  
A2 Receptors

The protective effect of ATP-MgCl2 on ischemia-reperfusion lung injury has been reported in kidney, liver, heart, and muscle but has not been examined in lungs. The aim of this study was to determine whether ATP or ATP-MgCl2 pretreatment would attenuate ischemia-reperfusion-induced acute lung injury and to identify the possible mechanisms for such protection. Typical acute lung injury was successfully induced in Sprague-Dawley rats by 10 min of hypoxia followed by 75 min of ischemia and 50 min of reperfusion. Pretreatment with ATP-MgCl2 (or adenosine) but not ATP or MgCl2 (all at 10(-6) M) significantly attenuated the acute lung injury. All the protective effects of ATP-MgCl2 were nearly undetectable when promazine (an ecto-adenosinetriphosphatase inhibitor) or 3,7-dimethyl-1-propargylxanthine (an A2-receptor antagonist) was added before ATP-MgCl2 pretreatment. These observations support our hypothesis that the protective effect of ATP-MgCl2 is in part mediated through adenosine, the degradation product of ATP, which is produced by the Mg(2+)-dependent ecto-adenosinetriphosphatase on the surface of neutrophils and reacts with neutrophil A2 receptors to inhibit the production of O2 radicals.

Lung injury after silica instillation is associated with an accumulation of iron in rats

1994 ◽  
Vol 267 (6) ◽  
pp. L686-L692 ◽  
Author(s):  
A. J. Ghio ◽  
R. H. Jaskot ◽  
G. E. Hatch
Keyword(s):  
Lung Injury ◽  
Lung Tissue ◽  
Liver Tissue ◽  
Oxidant Stress ◽  
Lavage Fluid ◽  
Sprague Dawley ◽  
Iron Stores ◽  
Silica Dust ◽  
Oxidized Products

It has been postulated that the incomplete complexation of host iron by the surface of mineral oxides is essential in in vivo lung injury after exposure to these dusts. We investigated the associations between in vivo iron accumulation after intratracheal instillation of silica dust in rats and 1) concentrations of antioxidants and oxidized products in the lung and 2) an index of chronic fibrotic injury. Fifty milligrams of minusil were intratracheally instilled into 60-day-old, male Sprague-Dawley rats. Ionizable Fe3+ complexed to the surface of silica increased from 12.7 +/- 1.4 mumol/g to values as high as 42.5 +/- 9.1 mumol/g dust after instillation. Corresponding to this elevation of surface-adsorbed metal, concentrations of iron in bronchoalveolar lavage fluid, lung tissue, plasma, and liver tissue all increased. Antioxidant molecules in lung tissue, including ascorbate, urate, and glutathione, all decreased, whereas superoxide dismutase increased. Oxidized products in the lung tissue, measured as thiobarbituric acid-reactive products, similarly increased, reflecting an oxidant stress. Dietary depletion of iron stores before instillation of silica dust resulted in low iron stores (hematocrit values of 21.8 +/- 1.9) and low iron concentrations in lavage fluid, lung tissue, and liver tissue. Rats on iron-depleted diets demonstrated a diminished fibrotic injury after dust instillation. Complexation of iron by the dust surface may be central in collagen deposition after silica exposure.

Dibutyryl cyclic GMP and hyperventilation promote rat lung phospholipid release

1979 ◽  
Vol 47 (2) ◽  
pp. 285-289 ◽  
Author(s):  
D. J. Klass
Keyword(s):  
Pulmonary Artery ◽  
Lung Tissue ◽  
Lavage Fluid ◽  
Rat Lung ◽  
Sprague Dawley ◽  
Fourth Group ◽  
Cyclic Monophosphate ◽  
Sprague Dawley Rats ◽  
Increased Pressure ◽  
Lung Phospholipid

Ventilation of rats at high inspiratory pressures raises lung tissue content of guanosine 30,5′-cyclic monophosphate (cGMP). Hyperventilation in rabbits augments release of phospholipid into lavage fluid. Can cGMP, in the absence of hyperventilation, increase lung phospholipid release? Sprague-Dawley rats are injected with [14C]palmitate, and after 1.5 h are anesthetized and ventilated for 20 min. Three groups are ventilated at peak inspiratory pressures (PIP) of 10 cmH2O, while saline, dibutyryl adenosine 3′,5′-cyclic monophosphate (DBcAMP), or dibutyryl cGMP (DBcGMP) is infused into the pulmonary artery. In a fourth group, saline is infused into the pulmonary artery, but ventilation is performed with PIP of 25 cmH2O. Lung tissue and lavage fluid are then analyzed for phospholipid (PL) content and for incorporation of [14C]palmitate into lavage and tissue PL fractions. Ventilation at increased pressure and infusion of DBcGMP are associated with increases in release of labeled PL into lavage fraction. The findings suggest that the increase in lavage PL release associated with hyperventilation is, at least in part, mediated by cGMP.

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