Protective effects of hydrogen against irradiation

2021 ◽  
Vol 27 ◽  
Author(s):  
Yasuhiro Terasaki ◽  
Mika Terasaki ◽  
Akira Shimizu
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Cultured Cells ◽  
Animal Experiments ◽  
Lung Epithelial Cells ◽  
Lung Damage ◽  
Protective Effects ◽  
Chronic Radiation ◽  
Radiation Induced ◽  
Reactive Oxidants

: Radiation-induced lung injury is characterized by an acute pneumonia phase followed by a fibrotic phase. At the time of irradiation, a rapid, short-lived burst of reactive oxygen species (ROS) such as hydroxyl radicals (•OH) occurs, but chronic radiation-induced lung injury may occur due to excess ROS such as H2O2 , O2•− , ONOO− , and •OH. Molecular hydrogen (H2 ) is an efficient antioxidant that quickly diffuses cell membranes, reduces ROS such as •OH and ONOO− , and suppresses damage caused by oxidative stress in various organs. In 2011, through the evaluation of electron-spin resonance and fluorescent indicator signals, we had reported that H2 can eliminate •OH and can protect against oxidative stress-related apoptotic damage induced by irradiation of cultured lung epithelial cells. We had explored for the first time the radioprotective effects of H2 treatment on acute and chronic radiation-induced lung damage in mice by inhaled H2 gas (for acute) and imbibed H2 -enriched water (for chronic). Thus, we had proposed that H2 be considered a potential radioprotective agent. Recent publications have shown that H2 directly neutralizes highly reactive oxidants and indirectly reduces oxidative stress by regulating the expression of various genes. By regulating gene expression, H2 functions as an anti-inflammatory and anti-apoptotic molecule and promotes energy metabolism. The increased evidence obtained from cultured cells or animal experiments reveal a putative place for H2 treatment and its radioprotective effect clinically. This review focuses on major scientific advances of in the treatment of H2 as a new class of radioprotective agents.

scholarly journals Acetylated Polysaccharides From Pleurotus geesteranus Alleviate Lung Injury Via Regulating NF-κB Signal Pathway

2020 ◽  
Vol 21 (8) ◽  
pp. 2810
Author(s):  
Xinling Song ◽  
Jianjun Zhang ◽  
Jian Li ◽  
Le Jia
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Animal Experiments ◽  
Immunofluorescence Assay ◽  
Signal Pathway ◽  
Lung Damage ◽  
Natural Food ◽  
Lung Protection ◽  
Tnf Α ◽  
Lung Functions

The present work investigated the anti-inflammatory, antioxidant, and lung protection effects of acetylated Pleurotus geesteranus polysaccharides (AcPPS) on acute lung injury (ALI) mice. The acetylation of AcPPS was successfully shown by the peaks of 1737 cm−1 and 1249 cm−1 by FTIR. The animal experiments demonstrated that lung damage can be induced by zymosan. However, the supplementation of AcPPS had potential effects on reducing lung index, remitting inflammatory symptoms (TNF-α, IL-1β, and IL-6), inhibiting NF-κB signal pathway based on up-regulating the level of IκBα and down-regulating p-IκBα level by Western blotting and immunofluorescence assay, preventing oxidative stress (ROS, SOD, GSH-Px, CAT, T-AOC, and MDA), reducing lipid accumulation (TC, TG, LDL-C, HDL-C, and VLDL-C), and alleviating lung functions by histopathologic observation. These results demonstrated that AcPPS might be suitable for natural food for prevention or remission in ALI.

Protective effects of molecular hydrogen on lung injury from lung transplantation

2021 ◽  
pp. 153537022110070
Author(s):  
Lini Quan ◽  
Bin Zheng ◽  
Huacheng Zhou
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Lung Transplantation ◽  
Animal Experiments ◽  
Multiple Organ ◽  
Protective Effects ◽  
Regulatory Molecule ◽  
Underlying Mechanisms ◽  
Species Production ◽  
Transplant Complications

Lung grafts may experience multiple injuries during lung transplantation, such as warm ischaemia, cold ischaemia, and reperfusion injury. These injuries all contribute to primary graft dysfunction, which is a major cause of morbidity and mortality after lung transplantation. As a potential selective antioxidant, hydrogen molecule (H2) protects against post-transplant complications in animal models of multiple organ transplantation. Herein, the authors review the current literature regarding the effects of H2 on lung injury from lung transplantation. The reviewed studies showed that H2 improved the outcomes of lung transplantation by decreasing oxidative stress and inflammation at the donor and recipient phases. H2 is primarily administered via inhalation, drinking hydrogen-rich water, hydrogen-rich saline injection, or a hydrogen-rich water bath. H2 favorably modulates signal transduction and gene expression, resulting in the suppression of pro-inflammatory cytokines and excess reactive oxygen species production. Although H2 appears to be a physiological regulatory molecule with antioxidant, anti-inflammatory and anti-apoptotic properties, its exact mechanisms of action remain elusive. Taken together, accumulating experimental evidence indicates that H2 can significantly alleviate transplantation-related lung injury, mainly via inhibition of inflammatory cytokine secretion and reduction in oxidative stress through several underlying mechanisms. Further animal experiments and preliminary human clinical trials will lay the foundation for the use of H2 as a treatment in the clinic.

Evaluation of Protective Effects of Curcumin and Nanocurcumin on Aluminium Phosphide‑Induced Subacute Lung Injury in Rats: Modulation of Oxidative Stress through SIRT1/FOXO3 Signalling Pathway

Drug Research ◽  
2021 ◽  
Author(s):  
Mohammad Ali Mahlooji ◽  
Ali Heshmati ◽  
Nejat Kheiripour ◽  
Hassan Ghasemi ◽  
Sara Soleimani Asl ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Lung Injury ◽  
Underlying Mechanism ◽  
Lung Damage ◽  
Pcr Analysis ◽  
Protective Effects ◽  
Aluminum Phosphide ◽  
Oxidative Stress Biomarkers ◽  
Genes Expression

Abstract Objective Aluminum phosphide (AlP) is widely used to protect stored food products and grains from pests and rodents. The availability of AlP, especially in Asian countries it has become a desirable factor to commit suicide. The phosphine produced from ALP is a very reactive radical and a respiratory inhibitor that causes oxidative damage. There is no dedicated antidote or effective drug to manage AlP-induced lung toxicity. The present study aims to evaluate and compare the protective effects of curcumin and nanocurcumin on ALP‑induced subacute lung injury and determine the underlying mechanism. Methods Rats were exposed to AlP (2 mg/kg/day, orally)+curcumin or nanocurcumin (100 mg/kg/day, orally) for 7 days. Then rats were anesthetized and lung tissues were collected. Oxidative stress biomarkers, genes expression of antioxidant enzymes, participated genes in the SIRT1/FOXO3 pathway, and lung histopathology were assessed by biochemical and ELISA methods, Real-Time PCR analysis, and H&E staining. Results Curcumin and nanocurcumin produced a remarkable improvement in AlP-induced lung damage through reduction of MDA, induction of antioxidant capacity (TAC, TTG) and antioxidant enzymes (CAT, GPx), modulation of histopathological changes, and up-regulation of genes expression of SIRT1, FOXO3, FOXO1 in lung tissue. Conclusion Nanocurcumin had a significantly more protective effect than curcumin to prevent AlP-induced lung injury via inhibition of oxidative stress. Nanocurcumin could be considered a suitable therapeutic choice for AlP poisoning.

Topiroxostat ameliorates oxidative stress and inflammation in sepsis-induced lung injury

2020 ◽  
Vol 75 (11-12) ◽  
pp. 425-431
Author(s):  
Haiying Fu ◽  
Junjie Zhang ◽  
Mayu Huang
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Vital Role ◽  
Lung Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Chemotactic Protein ◽  
Apoptosis Protein ◽  
Factor Α ◽  
Related Proteins

AbstractSepsis-induced lung injury was the most common cause of death in patients. Topiroxostat, a novel xanthine oxidoreductase inhibitors, possessed obvious organ protectives effects. Xanthine oxidase played a vital role in acute lung injury. The study aimed to investigate the roles of Topiroxostat in sepsis-induced lung injury. The sepsis rats were established using cecum ligation and perforation. The lung damage induced by sepsis was evaluated by Hematoxylin and Eosin staining and lung tissue wet to dry ratio. The oxidative stress was detected by measurement of reactive oxygen species, malondialdehyde, myeloperoxidase and superoxide dismutase (SOD). The pro-inflammatory mediators, tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and monocyte chemotactic protein 1, were measured by Enzyme-Linked Immunosorbent Assay. The cell apoptosis in lung was detected by TUNNEL staining and western blot analysis of apoptosis-related proteins including pro-apoptosis proteins, Bax, cleaved caspase9, cleaved caspase3 and anti-apoptosis protein Bcl2. The results showed that Topiroxostat significantly reduced lung damage, along with decreased oxidative stress, inflammation response and apoptosis in sepsis rats. Topiroxostat exerted markedly protective effects in sepsis-induced lung injury and could be an antioxidant in treating sepsis-induced lung injury.

scholarly journals Tomatidine Improves Pulmonary Inflammation in Mice with Acute Lung Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Wen-Chung Huang ◽  
Shu-Ju Wu ◽  
Ya-Ling Chen ◽  
Chwan-Fwu Lin ◽  
Chian-Jiun Liou
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Tissue ◽  
Inflammatory Cytokine ◽  
Animal Experiments ◽  
Intratracheal Instillation ◽  
Lung Epithelial Cells ◽  
Mitogen Activated Protein Kinase ◽  
Heme Oxygenase 1

Tomatidine, which is isolated from green tomato, can ameliorate inflammation and oxidative stress in cells and animal experiments and has been shown to improve airway inflammation in a murine model of asthma. Here, we investigated whether tomatidine can ameliorate acute lung injury in mice. Mice were given tomatidine by intraperitoneal injection for 7 consecutive days, and then, lung injury was induced via intratracheal instillation of lipopolysaccharide (LPS). Tomatidine reduced inflammatory cytokine expressions in bronchoalveolar lavage fluid (BALF), attenuated neutrophil infiltration in the BALF and lung tissue, increased superoxide dismutase activity and glutathione levels, and alleviated myeloperoxidase expression in the lung tissue of mice with lung injury. Tomatidine also decreased inflammatory cytokine and chemokine gene expression in inflammatory lungs and attenuated the phosphorylation of mitogen-activated protein kinase and nuclear factor kappa B. Furthermore, tomatidine enhanced the production of heme oxygenase-1, decreased the secretion of inflammatory cytokines and chemokines in LPS-stimulated lung epithelial cells, and attenuated THP-1 monocyte adhesion. Our findings suggest that tomatidine attenuates oxidative stress and inflammation, improving acute lung injury in mice.

Ionizing radiation enhances matrix metalloproteinase-2 production in human lung epithelial cells

2001 ◽  
Vol 280 (1) ◽  
pp. L30-L38 ◽  
Author(s):  
Jun Araya ◽  
Muneharu Maruyama ◽  
Kazuhiko Sassa ◽  
Tadashi Fujita ◽  
Ryuji Hayashi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Ionizing Radiation ◽  
Basement Membrane ◽  
Lung Injury ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Radiation Induced ◽  
Human Lung Epithelial Cells

Radiation pneumonitis is a major complication of radiation therapy. However, the detailed cellular mechanisms have not been clearly defined. Based on the recognition that basement membrane disruption occurs in acute lung injury and that matrix metalloproteinase (MMP)-2 can degrade type IV collagen, one of the major components of the basement membrane, we hypothesized that ionizing radiation would modulate MMP-2 production in human lung epithelial cells. To evaluate this, the modulation of MMP-2 with irradiation was investigated in normal human bronchial epithelial cells as well as in A549 cells. We measured the activity of MMP-2 in the conditioned medium with zymography and the MMP-2 mRNA level with RT-PCR. Both of these cells constitutively expressed 72-kDa gelatinolytic activity, corresponding to MMP-2, and exposure to radiation increased this activity. Consistent with the data of zymography, ionizing radiation increased the level of MMP-2 mRNA. This radiation-induced increase in MMP-2 expression was mediated via p53 because the p53 antisense oligonucleotide abolished the increase in MMP-2 activity as well as the accumulation of p53 after irradiation in A549 cells. These results indicate that MMP-2 expression by human lung epithelial cells is involved in radiation-induced lung injury.

scholarly journals Inhibition of Rac1 attenuates radiation-induced lung injury while suppresses lung tumor in mice

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Ni An ◽  
Zhenjie Li ◽  
Xiaodi Yan ◽  
Hainan Zhao ◽  
Yajie Yang ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Lung Injury ◽  
Mouse Model ◽  
Tumor Cells ◽  
Nuclear Translocation ◽  
Lung Tumor ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Limiting Factor ◽  
Radiation Induced

AbstractThe lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.

Radioprotective effect of diethylcarbamazine on radiation-induced acute lung injury and oxidative stress in mice

2019 ◽  
Vol 52 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Soghra Farzipour ◽  
Fereshteh Talebpour Amiri ◽  
Ehsan Mihandoust ◽  
Fatemeh Shaki ◽  
Zohreh Noaparast ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Radioprotective Effect ◽  
Radiation Induced ◽  
And Oxidative Stress

scholarly journals Protective Effects of Myrtol Standardized Against Radiation-Induced Lung Injury

2016 ◽  
Vol 38 (2) ◽  
pp. 619-634 ◽  
Author(s):  
De-yun Zhao ◽  
Hong-jin Qu ◽  
Jia-ming Guo ◽  
Hai-nan Zhao ◽  
Yan-yong Yang ◽  
...  
Keyword(s):  
Single Dose ◽  
Lung Injury ◽  
Major Complication ◽  
The Body ◽  
Protective Effects ◽  
Western Blot Assay ◽  
Tnf Α ◽  
Radiation Induced ◽  
The Impact ◽  
Tgf Β1

Background/Aims: As a major complication after thoracic radiotherapy, radiation-induced lung injury (RILI) has great impact on long term quality of life and could result in fatal respiratory insufficiency The present study was aimed to evaluate the effects of Myrtol standardized on RILI, and to investigate the underlying mechanism. Methods: A mouse model of radiation-induced lung injury was generated by using thoracic irradiation with a single dose of 16Gy. Mice were orally administrated with Myrtol (25 mg/kg/day) for 4 weeks after irradiation, while prednisone (5 mg/kg/day) was used as a positive control. After then, the body weight and lung coefficient were calculated. The severity of fibrosis was evaluated by observing pulmonary sections after radiation and collagen content in lung tissues was calculated following the hydroxyproline (HYP) assay. Pathological changes were observed in all the groups by using HE staining and Masson staining. The serum levels of TGF-β1, TNF-α, IL-1β, IL-6, and PGE2 were also measured with an ELISA assay. Western blot assay was used to measure the impact of Myrtol on AKT and its downstream signaling pathway, including MMP-2 and MMP-9. The levels of Vimentin and α-SMA were evaluated with an immunofluorescence assay. Results: Treatment with Myrtol standardized, but not prednisone, reduced lung coefficient and collagen deposition in lung tissues, while attenuated histological damages induced by irradiation. Myrtol standardized also reduced the production of MDA, while increased the level of SOD. It was also observed that Myrtol standardized inhibited TGF-β1 and a series of pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, PGE2. While in prednisone group, even though the early pneumonitis was ameliorated, the collagen disposition remained unchanged in latter times. Immunofluorescence analysis also revealed elevation of vimentin and α-SMA in the alveoli after a single dose of 16Gy. Conclusion: The present results suggest Myrtol standardized as an effective agent for attenuating the lung injury induced by irradiation.

PECAM-directed delivery of catalase to endothelium protects against pulmonary vascular oxidative stress

2003 ◽  
Vol 285 (2) ◽  
pp. L283-L292 ◽  
Author(s):  
Melpo Christofidou-Solomidou ◽  
Arnaud Scherpereel ◽  
Rainer Wiewrodt ◽  
Kimmie Ng ◽  
Thomas Sweitzer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Intravenous Injection ◽  
Targeted Delivery ◽  
Ischemia Reperfusion ◽  
Therapeutic Interventions ◽  
Protective Effects ◽  
Stress Injury ◽  
Pulmonary Endothelium

Targeted delivery of drugs to vascular endothelium promises more effective and specific therapies in many disease conditions, including acute lung injury (ALI). This study evaluates the therapeutic effect of drug targeting to PECAM (platelet/endothelial cell adhesion molecule-1) in vivo in the context of pulmonary oxidative stress. Endothelial injury by reactive oxygen species (e.g., H2O2) is involved in many disease conditions, including ALI/acute respiratory distress syndrome and ischemia-reperfusion. To optimize delivery of antioxidant therapeutics, we conjugated catalase with PECAM antibodies and tested properties of anti-PECAM/catalase conjugates in cell culture and mice. Anti-PECAM/catalase, but not an IgG/catalase counterpart, bound specifically to PECAM-expressing cells, augmented their H2O2-degrading capacity, and protected them against H2O2 toxicity. Anti-PECAM/catalase, but not IgG/catalase, rapidly accumulated in the lungs after intravenous injection in mice, where it was confined to the pulmonary endothelium. To test its protective effect, we employed a murine model of oxidative lung injury induced by glucose oxidase coupled with thrombomodulin antibody (anti-TM/GOX). After intravenous injection in mice, anti-TM/GOX binds to pulmonary endothelium and produces H2O2, which causes lung injury and 100% lethality within 7 h. Coinjection of anti-PECAM/catalase protected against anti-TM/GOX-induced pulmonary oxidative stress, injury, and lethality, whereas polyethylene glycol catalase or IgG/catalase conjugates afforded only marginal protective effects. This result validates vascular immunotargeting as a prospective strategy for therapeutic interventions aimed at immediate protective effects, e.g., for augmentation of antioxidant defense in the pulmonary endothelium and treatment of ALI.

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