Measurements for Sulfide-Mediated Inhibition of Myeloperoxidase Activity

2019 ◽  
pp. 179-203
Author(s):  
Dorottya Garai ◽  
Zoltán Pálinkás ◽  
József Balla ◽  
Anthony J. Kettle ◽  
Péter Nagy
Keyword(s):  
Myeloperoxidase Activity

Juglone Attenuates Sepsis-Induced Acute Lung Injury via Suppression of the TLR4/Nf-κb Pathway

2020 ◽  
Vol 18 (2) ◽  
pp. 201-206
Author(s):  
Qiu Nan ◽  
Xu Xinmei ◽  
He Yingying ◽  
Fan Chengfen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Nuclear Factor Kappa B ◽  
Cecal Ligation ◽  
Myeloperoxidase Activity ◽  
Nuclear Factor ◽  
Cecal Ligation And Puncture ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nuclear Factor Kappa

Sepsis, with high mortality, induces deleterious organ dysfunction and acute lung injury. Natural compounds show protective effect against sepsis-induced acute lung injury. Juglone, a natural naphthoquinone, demonstrates pharmacological actions as a pro-apoptotic substrate in tumor treatment and anti-inflammation substrate in organ injury. In this study, the influence of juglone on sepsis-induced acute lung injury was investigated. First, a septic mice model was established via cecal ligation and puncture, and then verified via histopathological analysis of lung tissues, the wet/dry mass ratio and myeloperoxidase activity was determined. Cecal ligation and puncture could induce acute lung injury in septic mice, as demonstrated by alveolar damage and increase of wet/dry mass ratio and myeloperoxidase activity. However, intragastric administration juglone attenuated cecal ligation and puncture-induced acute lung injury. Secondly, cecal ligation and puncture-induced increase of inflammatory cells in bronchoalveolar lavage fluid was also alleviated by the administration of juglone. Similarly, the protective effect of juglone against cecal ligation and puncture-induced acute lung injury was accompanied by a reduction of pro-inflammatory factor secretion in bronchoalveolar lavage fluid and lung tissues. Cecal ligation and puncture could activate toll-like receptor 4/nuclear factor-kappa B signaling pathway, and administration of juglone suppressed toll-like receptor 4/nuclear factor-kappa B activation. In conclusion, juglone attenuated cecal ligation and puncture-induced lung damage and inflammatory response through inactivation of toll-like receptor 4/nuclear factor-kappa B, suggesting a potential therapeutic strategy in the treatment of sepsis-induced acute lung injury.

Oxygen radicals trigger activation of NF-κB and AP-1 and upregulation of ICAM-1 in reperfused canine heart

2002 ◽  
Vol 282 (5) ◽  
pp. H1778-H1786 ◽  
Author(s):  
Haiying Fan ◽  
Baogui Sun ◽  
Qiuping Gu ◽  
Anne Lafond-Walker ◽  
Suyi Cao ◽  
...  
Keyword(s):  
Dna Binding ◽  
Protein Expression ◽  
Vascular Endothelium ◽  
Oxygen Radicals ◽  
Nuclear Dna ◽  
Ischemia Reperfusion ◽  
Intercellular Adhesion Molecule ◽  
Radical Scavenger ◽  
Myeloperoxidase Activity ◽  
Canine Heart

We investigated whether oxygen radicals generated during ischemia-reperfusion trigger postischemic inflammation in the heart. Closed-chest dogs underwent 90-min coronary artery occlusion, followed by 1- or 3-h reperfusion: 10 dogs received the cell-permeant oxygen radical scavenger N-(2-mercaptopropionyl)-glycine (MPG; 8 mg · kg−1 · h−1intracoronary) beginning 5 min before reperfusion, and 9 dogs received vehicle. Blood flow (microspheres), intercellular adhesion molecule (ICAM)-1 protein expression (immunohistochemistry), ICAM-1 gene activation (Northern blotting), nuclear DNA binding activity of nuclear factor (NF)-κb and AP-1 (electrophoretic mobility shift assays), and neutrophil (PMN) accumulation (myeloperoxidase activity) were assessed in myocardial tissue samples. ICAM-1 protein expression was high in vascular endothelium after ischemia-reperfusion but was markedly reduced by MPG. MPG treatment also markedly decreased expression of ICAM-1 mRNA and tissue PMN accumulation. Nuclear DNA binding activities of NF-κB and AP-1, increased by ischemia-reperfusion, were both markedly decreased by MPG at 1 h of reperfusion. However, by 3 h, AP-1 activity was only modestly reduced by MPG and NF-κB activity was not significantly different from ischemic-reperfused controls. These results suggest that oxygen radicals generated in vivo during reperfusion trigger early activation of NF-κb and AP-1, resulting in upregulation of the ICAM-1 gene in vascular endothelium and subsequent tissue accumulation of activated PMNs.

scholarly journals Effects of Green Alga, Chaetomorpha aerea Extract on Non-Specific Immune Responses and Disease Resistance against Edwardsiella tarda Infection in Labeo rohita

2021 ◽  
Vol 11 (10) ◽  
pp. 4325
Author(s):  
Govindharajan Sattanathan ◽  
Vairakannu Tamizhazhagan ◽  
Nadeem Raza ◽  
Syed Qaswar Ali Shah ◽  
Muhammad Zubair Hussain ◽  
...  
Keyword(s):  
Immune Responses ◽  
Green Alga ◽  
Labeo Rohita ◽  
Virulent Strain ◽  
Edwardsiella Tarda ◽  
Fish Mortality ◽  
Control Group ◽  
Physiological Salt Solution ◽  
Myeloperoxidase Activity ◽  
Chaetomorpha Aerea

The current study evaluated the effects of a methanol extract from Chaetomorpha aerea (a green alga) on non-specific immune responses and resistance against Edwardsiella tarda infection in Labeo rohita. Different doses of the extract (5, 50 and 500 mg/kg of body weight) were injected into the fish intraperitoneally while a control group was injected with 0.2 mL of sterile physiological salt solution. Variations in several immunostimulatory parameters (i.e., neutrophil, serum lysozyme, myeloperoxidase, serum antiprotease, and ceruloplasmin activity), reactive oxygen species (ROS) and reactive nitrogen species (RNS) were assessed after 7, 14, 21, and 28 days of post stimulation. E. tarda culture was injected into the fish after 28 days of post stimulation to induce infection to monitor fish mortality within 14 days. Interestingly, all doses of methanolic extract enhanced neutrophil, lysozyme, and myeloperoxidase activity, ROS and RNS, while a dose of 50 mg/kg was the most effective. Fish injected with this optimal dose were also protected against infection with virulent strain of E. tarda. The results of the study suggest that C. aerea extract is a potential prophylactic agent against bacterial infections in finfish.

scholarly journals Efficacy of Posidonia oceanica Extract against Inflammatory Pain: In Vivo Studies in Mice

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 48
Author(s):  
Laura Micheli ◽  
Marzia Vasarri ◽  
Emanuela Barletta ◽  
Elena Lucarini ◽  
Carla Ghelardini ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Ex Vivo ◽  
Antioxidant Properties ◽  
Posidonia Oceanica ◽  
In Vivo Studies ◽  
Myeloperoxidase Activity ◽  
Intraplantar Injection ◽  
Hot Plate Test ◽  
Anti Inflammatory

Posidonia oceanica (L.) Delile is traditionally used for its beneficial properties. Recently, promising antioxidant and anti-inflammatory biological properties emerged through studying the in vitro activity of the ethanolic leaves extract (POE). The present study aims to investigate the anti-inflammatory and analgesic role of POE in mice. Inflammatory pain was modeled in CD-1 mice by the intraplantar injection of carrageenan, interleukin IL-1β and formalin. Pain threshold was measured by von Frey and paw pressure tests. Nociceptive pain was studied by the hot-plate test. POE (10–100 mg kg−1) was administered per os. The paw soft tissue of carrageenan-treated animals was analyzed to measure anti-inflammatory and antioxidant effects. POE exerted a dose-dependent, acute anti-inflammatory effect able to counteract carrageenan-induced pain and paw oedema. Similar anti-hyperalgesic and anti-allodynic results were obtained when inflammation was induced by IL-1β. In the formalin test, the pre-treatment with POE significantly reduced the nocifensive behavior. Moreover, POE was able to evoke an analgesic effect in naïve animals. Ex vivo, POE reduced the myeloperoxidase activity as well as TNF-α and IL-1β levels; further antioxidant properties were highlighted as a reduction in NO concentration. POE is the candidate for a new valid strategy against inflammation and pain.

scholarly journals Host DNA Repair Proteins in Response toPseudomonas aeruginosain Lung Epithelial Cells and in Mice

2010 ◽  
Vol 79 (1) ◽  
pp. 75-87 ◽  
Author(s):  
Min Wu ◽  
Huang Huang ◽  
Weidong Zhang ◽  
Shibichakravarthy Kannan ◽  
Andrew Weaver ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Epithelial Cells ◽  
Critical Role ◽  
Lung Epithelial Cells ◽  
Host Cells ◽  
Myeloperoxidase Activity ◽  
Gram Negative ◽  
Lung Epithelial ◽  
Dna Repair Proteins

ABSTRACTAlthough DNA repair proteins in bacteria are critical for pathogens' genome stability and for subverting the host defense, the role of host DNA repair proteins in response to bacterial infection is poorly defined. Here, we demonstrate, for the first time, that infection with the Gram-negative bacteriumPseudomonas aeruginosasignificantly altered the expression and enzymatic activity of 8-oxoguanine DNA glycosylase (OGG1) in lung epithelial cells. Downregulation of OGG1 by a small interfering RNA strategy resulted in severe DNA damage and cell death. In addition, acetylation of OGG1 is required for host responses to bacterial genotoxicity, as mutations of OGG1 acetylation sites increased Cockayne syndrome group B (CSB) protein expression. These results also indicate that CSB may be involved in DNA repair activity during infection. Furthermore, OGG1 knockout mice exhibited increased lung injury after infection withP. aeruginosa, as demonstrated by higher myeloperoxidase activity and lipid peroxidation. Together, our studies indicate thatP. aeruginosainfection induces significant DNA damage in host cells and that DNA repair proteins play a critical role in the host response toP. aeruginosainfection, serving as promising targets for the treatment of this condition and perhaps more broadly Gram-negative bacterial infections.

Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection

2002 ◽  
Vol 282 (3) ◽  
pp. L563-L572 ◽  
Author(s):  
Ann Marie LeVine ◽  
Kevan Hartshorn ◽  
James Elliott ◽  
Jeffrey Whitsett ◽  
Thomas Korfhagen
Keyword(s):  
Lung Inflammation ◽  
Influenza A ◽  
Influenza Infection ◽  
Pulmonary Inflammation ◽  
Defense Responses ◽  
Interferon Γ ◽  
Viral Clearance ◽  
Myeloperoxidase Activity ◽  
Respiratory Pathogens ◽  
Innate Defense

Mice lacking surfactant protein SP-A [SP-A(−/−)] and wild type SP-A(+/+) mice were infected with influenza A virus (IAV) by intranasal instillation. Decreased clearance of IAV was observed in SP-A(−/−) mice and was associated with increased pulmonary inflammation. Treatment of SP-A(−/−) mice with exogenous SP-A enhanced viral clearance and decreased lung inflammation. Uptake of IAV by alveolar macrophages was similar in SP-A(−/−) and SP-A(+/+) mice. Myeloperoxidase activity was reduced in isolated bronchoalveolar lavage neutrophils from SP-A(−/−) mice. B lymphocytes and activated T lymphocytes were increased in the lung and spleen, whereas T helper (Th) 1 responses were increased [interferon-γ, interleukin (IL)-2, and IgG2a] and Th2 responses were decreased (IL-4, and IL-10, and IgG1) in the lungs of SP-A(−/−) mice 7 days after IAV infection. In the absence of SP-A, impaired viral clearance was associated with increased lung inflammation, decreased neutrophil myeloperoxidase activity, and increased Th1 responses. Because the airway is the usual portal of entry for IAV and other respiratory pathogens, SP-A is likely to play a role in innate defense and adaptive immune responses to IAV.

TREATMENT OF MUCOCUTANEOUS CANDIDIASIS WITH TRANSFER FACTOR

PEDIATRICS ◽  
1974 ◽  
Vol 53 (1) ◽  
pp. 63-70
Author(s):  
Ralph D. Feigin ◽  
Penelope G. Shackelford ◽  
Seth Eisen ◽  
Lynn E. Spitler ◽  
Larry K. Pickering ◽  
...  
Keyword(s):  
Amphotericin B ◽  
Skin Test ◽  
Migration Inhibitory Factor ◽  
Transfer Factor ◽  
Chronic Mucocutaneous Candidiasis ◽  
Myeloperoxidase Activity ◽  
Mucocutaneous Candidiasis ◽  
Receptor Sites ◽  
Stimulation Of

Evaluation of a patient with chronic mucocutaneous candidiasis revealed that the patient lacked delayed hypersensitivity to candida and other skin test antigens and the patient's lymphocytes could not be stimulated in vitro with candida antigen. Phytohemagglutinin stimulation of lymphocytes in vitro was normal. Candidacidal function and myeloperoxidase activity of the patient's leukocytes were normal. The patient's lymphocytes produced migration inhibitory factor in response to candida antigen and the monocyte receptor sites for IgG were intact. Repeated treatments with amphotericin B, alone or with 5-fluorocytosine, were followed by immediate relapse. Four doses of transfer factor were administered and when coupled with amphotericin B on two occasions prompted remissions of 6 and 4 months, respectively.

CCSP modulates airway dysfunction and host responses in an Ova-challenged mouse model

2001 ◽  
Vol 281 (5) ◽  
pp. L1303-L1311 ◽  
Author(s):  
Shan-Ze Wang ◽  
Cynthia L. Rosenberger ◽  
Teresa M. Espindola ◽  
Edward G. Barrett ◽  
Yohannes Tesfaigzi ◽  
...  
Keyword(s):  
Airway Epithelium ◽  
Host Response ◽  
Secretory Protein ◽  
Allergic Airway Disease ◽  
Clara Cell ◽  
Myeloperoxidase Activity ◽  
Wild Type ◽  
Airway Reactivity ◽  
Mucus Production

Clara cell secretory protein (CCSP) is synthesized by nonciliated bronchiolar cells in the lung and modulates lung inflammation to infection. To determine the role of CCSP in the host response to allergic airway disease, CCSP-deficient [(−/−)] mice were immunized twice with ovalbumin (Ova) and challenged by Ova (2 or 5 mg/m3) aerosol. After 2, 3, and 5 days of Ova aerosol challenge (6 h/day), airway reactivity was increased in CCSP(−/−) mice compared with wild-type [CCSP(+/+)] mice. Neutrophils were markedly increased in the bronchoalveolar lavage fluid of CCSP(−/−) Ova mice, coinciding with increased myeloperoxidase activity and macrophage inflammatory protein-2 levels. Lung histopathology and inflammation were increased in CCSP(−/−) compared with wild-type mice after Ova challenge. Mucus production, as assessed by histological staining, was increased in the airway epithelium of CCSP(−/−) Ova mice compared with that in CCSP(+/+) Ova mice. These data suggest a role for CCSP in airway reactivity and the host response to allergic airway inflammation and provide further evidence for the role of the airway epithelium in regulating airway responses in allergic disease.

Microcirculatory disturbance in indomethacin-induced intestinal ulcer

1991 ◽  
Vol 261 (2) ◽  
pp. G213-G219 ◽  
Author(s):  
S. Miura ◽  
M. Suematsu ◽  
S. Tanaka ◽  
H. Nagata ◽  
S. Houzawa ◽  
...  
Keyword(s):  
Intestinal Mucosa ◽  
Venous Blood ◽  
Leukotriene B4 ◽  
Ulcer Formation ◽  
Myeloperoxidase Activity ◽  
Neutrophil Accumulation ◽  
Intestinal Ulcer ◽  
Leukocyte Accumulation ◽  
Lipoxygenase Products ◽  
Microcirculatory Disturbances

Participation of microcirculatory disturbances, especially the role of 5-lipoxygenase products from neutrophils, was investigated in indomethacin (Indo)-induced ulcers of rat small intestine. After Indo treatment (20 mg/kg) in rats, small erosions appeared at 6 h and longitudinal ulcers developed 12 h later. At 6 and 12 h after Indo treatment, severe microcirculatory disturbances were observed under an intravital fluorescence microscope. Significant delay in the clearance and patchy pooling of injected fluorescein isothiocyanate-bovine serum albumin with sludge and stasis were observed in archade vessels of villi of Indo-treated rats. Increased numbers of sticking leukocytes were also detected along submucosal venules in these rats after the infusion of acridine orange. When regional venous blood was collected from the mesentery, a marked increase in neutrophil number and their increased production of oxygen-derived free radicals as determined by chemiluminescence assay were demonstrated at 6 h after Indo treatment. There was also a significant increase in myeloperoxidase activity of the intestinal mucosa at 6 and 12 h after Indo treatment, suggesting a significant neutrophil accumulation at this time. AA-861, a selective inhibitor of 5-lipoxygenase (80 mg/kg), attenuated these microcirculatory changes and neutrophil accumulation in the intestinal mucosa. AA-861 also significantly prevented the formation of intestinal ulcers induced by Indo. However, Indo-induced ulcer formation and leukocyte accumulation in submucosal venules were not attenuated by the treatment of Ono-1078, a potent antagonist of sulfidopeptide leukotrienes. From these observations, it is considered that microcirculatory disturbances, especially leukocyte accumulation and 5-lipoxygenase products, possibly leukotriene B4, may be involved in the development of Indo-induced intestinal ulcer.

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