• Journal of Veterinary Clinics
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• v.25 no.2
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• pp.73-78
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• 2008

Ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist and a short-acting general anaesthetic agent for human and veterinary use. We previously reported that treatment with ketamine impairs oxidative burst activity of canine peripheral blood leukocytes. In this study, the effect of ketamine on phagocytic capacity of canine peripheral blood leukocytes was examined in vitro. Phagocytic capacity was analyzed by using a flow cytometry. Ketamine directly decreased the phagocytic capacity of peripheral blood polymorphonuclear cells (PMN) and monocytes but not total peripheral blood mononuclear cells (PBMC). In addition, the phagocytic capacity of PMN and monocytes was inhibited by the ketamine-treated PBMC but not PMN culture supernatant. These results suggest that ketamine has a direct inhibitory effect on the phagocytic capacity of canine peripheral blood phagocytes and involves the production of soluble factor(s) from canine PBMC, which may suppress the phagocytic capacity.

• Journal of Chest Surgery
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• v.35 no.5
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• pp.343-349
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• 2002

background: In an attempt to investigate the role of oxidants in the activation of phospholipase $A_2$(PLA$_2$) and endogenous oxidative stress in the lung. acute inflammatory lung injury was induced by the instillation of hydrogen peroxide into the trachea of Sprague-Dawley rats. Material and Method: To prove the hypothesis thats released oxidants from neutrophils activate the PLA$_2$ retrogradely, activities of PLA$_2$ and lysoplatelet activating factor acetyltransferase(lysoPAF AT) were assayed i hours after instillation of hydrogen peroxide. In addition, to confirm the impairing effects of the activation of PLA$_2$ associated with endogenous oxidative stress, lung weight/body weight ratio(L$\times$10$^{-3}$ B), protein contents(mg/two lungs) in bronchoalveolar lavage(BAL) were measured. As neutrophilic respiratory burst has been known to play a pivotal role in the genesis of endogenous oxidative stress associated with acute inflammatory lung injury, BAL neutrophils counts and level of lung myelperoxidase(MPO) were measured after hydorgen peroxide insult. Morphological and histochemical studies were also performed to identify the effect of the endogenous oxidative stress. Result: Five hours after hydrogen peroxide instillation, lungs showed marked infiltration of neutrophils and increased weight. Protein contents in BAL increased significantly compared to those of normal rats. PLA$_2$ activity was enhanced in the hydrogen peroxide instilled group. Interestingly, the accelerated production of platelet activating factor(PAF) was confirmed by the increased activity of lysoPAF AT in the $H_2O$$_2$ employed lung. Morphologically, light microscopic findings of lungs after instillation of hydrogen peroxide showed atelectasis and infiltration of inflammatory cells, which was thought to be caused by lipid mediators produced by PLA$_2$ activation. In cerium chloride cytochemical electron microscopy, dense deposits of cerrous perhydroxide were identified. In contrast, no deposit of cerrous perhydroxide was found in the normal lung.

• Tuberculosis and Respiratory Diseases
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• v.68 no.6
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• pp.334-344
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• 2010

Background: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. Methods: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, $30{\mu}L$) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. Results: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and $CeCl_3$ EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase $A_2$ ($sPLA_2$) by OA. Conclusion: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of $sPLA_2$.

• Journal of Life Science
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• v.22 no.10
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• pp.1352-1358
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• 2012

In acute lung injury (ALI) by lipopolysaccharide (LPS), the underlying cause of infiltration and migration of neutrophils into the alveoli is considered to be from increased production of platelet-activating factor (PAF) in the pulmonary surfactant lining the alveolar lumen. In this study I partially confirmed this concept. LPS increased lung leak and the infiltration of neutrophils in the lung of rats given LPS intratracheally. The migration of neutrophils into the lung, which had caused oxidative stress, was also morphologically identified. I verified that the metabolism of the pulmonary surfactant was affected and that there was increased production of PAF in the pulmonary surfactant, both of which are considered to contribute to ALI by LPS in rats.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.6
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• pp.1495-1499
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• 2008

The purpose of this study is to investigate the effect of water extract from Artemisiae Argi Folium (WAAF) on hydrogen peroxide production within mouse macrophage Raw 264.7 Cells treated with gallic acid, EtOH, LPS, and acetaminophen. WAAF (0${\sim}$400 ug/mL) was treated with gallic acid, EtOH, LPS, acetaminophen. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. WAAF showed the restoration of the intracellular productions of hydrogen peroxide which were reduced by gallic acid, EtOH, LPS, and acetaminophen in Raw 264.7 Cells. WAAF could be supposed to have the immunological activity related with macrophage's oxidative burst.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1049-1054
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• 2009

The effect of Sacchromyces cerevisiae-Fermented Sophorae Radix water extract (SFS) on production of hydrogen peroxide and nitric oxide (NO) from mouse macrophage Raw 264.7 Cells treated with nicotine (1 mM) was investigated through this study. SFS (0, 25, 50, 100, 200, 400 ug/mL) was simultaneously treated with nicotine (1 mM) during culture of 4, 20, 24, 44, 48, 68, and 72 hr. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. NO production after 24 hr treatement was measured with Griess reagent assay. SFS restored the production of hydrogen peroxide and NO reduced by nicotine (1 mM) in Raw 264.7 Cells. These results suggests that SFS could be supposed to have the immunological activity concerned with macrophage's oxidative burst including hydrogen peroxide and NO.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.2
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• pp.438-442
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• 2009

The purpose of this study is to investigate the effect of water extract from Artemisiae Argi Folium Fermented with Lactobacillus pentosus (AFL) on hydrogen peroxide production within mouse macrophage Raw 264.7 Cells treated with gallic acid, EtOH, Nicotine, Acetaminophen, and Acetaldehyde. AFL (0${\sim}$400 ug/mL) was treated with gallic acid, EtOH, Nicotine, Acetaminophen, and Acetaldehyde. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. AFL showed the restoration of the intracellular productions of hydrogen peroxide which were reduced by gallic acid, EtOH, Nicotine, Acetaminophen in Raw 264.7 Cells. AFL could be supposed to have the immunological activity related with macrophage's oxidative burst.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.3
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• pp.608-612
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• 2009

The effect of Sacchromyces cerevisiae-Fermented Artemisiae Argi Folium Water extract (AFS) on hydrogen peroxide production within mouse macrophage Raw 264.7 Cells treated with EtOH, gallic acid, Nicotine, Acetaminophen, and Acetaldehyde was investigated through this study. AFS (0-400 ug/mL) was simultaneously treated with EtOH, gallic acid, Nicotine, Acetaminophen, and Acetaldehyde. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. AFS restorated the intracellular productions of hydrogen peroxide reduced by EtOH, gallic acid, Nicotine, Acetaminophen within Raw 264.7 Cells. AFS could be supposed to have the immunological activity concerned with macrophage's oxidative burst.

• The Plant Pathology Journal
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• v.20 no.1
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• pp.7-12
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• 2004

An important recent advance in the field of plant-microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or insects. Disease resistance (R) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. Plant disease resistance is the result of an innate host defense mechanism, which relies on the ability of plant to recognize pathogen invasion and efficiently mount defense responses. In tomato, resistance to the pathogen Pseudomonas syringae pv. tomato is mediated by the specific recognition between the tomato serine/threonine kinase Pto and bacterial protein AvrPto or AvrPtoB. This recognition event initiates signaling events that lead to defense responses including an oxidative burst, the hypersensitive response (HR), and expression of pathogenesis- related genes.

• Bulletin of the Korean Chemical Society
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• v.30 no.10
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• pp.2294-2298
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• 2009

In present work an attempt was made to synthesize various analogues of levofloxacin by introducing new functionality at carboxylic group position via nucleophilic substitution reaction. For this purpose the carboxylic group at C-6 was esterified and later subjected to nucleophilic attack at the carbonyl carbon by various aromatic amines. Structure of the analogues was confirmed by different techniques i.e. IR, $^1H$ NMR and mass spectrometry. The antibacterial activity of the derivatives was also assessed and compared with the parent against a series of Gram-positive and Gramnegative bacteria. A synergistic as well as antagonistic behavior was observed in these derivatives. Additionally unlike levofloxacin, the derivatives were also found to modulate oxidative burst response of phagocytes exhibiting moderate to significant inhibitory activity.