The Experts below are selected from a list of 48426 Experts worldwide ranked by ideXlab platform
Masao Nagumo - One of the best experts on this subject based on the ideXlab platform.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International Immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Kondo, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 μg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1β, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-α (TNF-α) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Gen Kondo, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 microg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1beta, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-alpha (TNF-alpha) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
Toru Kimura - One of the best experts on this subject based on the ideXlab platform.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International Immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Kondo, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 μg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1β, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-α (TNF-α) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Gen Kondo, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 microg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1beta, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-alpha (TNF-alpha) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
Daisuke Ito - One of the best experts on this subject based on the ideXlab platform.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International Immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Kondo, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 μg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1β, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-α (TNF-α) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Gen Kondo, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 microg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1beta, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-alpha (TNF-alpha) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
Masayasu Iwase - One of the best experts on this subject based on the ideXlab platform.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International Immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Kondo, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 μg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1β, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-α (TNF-α) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Gen Kondo, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 microg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1beta, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-alpha (TNF-alpha) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
Hitoshi Watanabe - One of the best experts on this subject based on the ideXlab platform.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International Immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Kondo, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 μg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1β, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-α (TNF-α) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
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Suppressive effect of selective cyclooxygenase-2 inhibitor on Cytokine Release in human neutrophils.
International immunopharmacology, 2003Co-Authors: Toru Kimura, Masayasu Iwase, Hitoshi Watanabe, Masaru Ohashi, Daisuke Ito, Gen Kondo, Masao NagumoAbstract:To clarify whether a selective cyclooxygenase-2 (COX-2) inhibitor can affect various functions in human peripheral blood neutrophils. For this purpose, the effects of selective COX-2 inhibitors, NS-398 and nimesulide, on the expression of COX-2, PGE2 Release and respiratory burst, degranulation and Cytokine Release in activated neutrophils were examined. Peripheral blood neutrophils were stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP; 100 nM) or opsonized zymosan (OZ; 200 microg/ml). Then, the expression of COX-2 at protein and mRNA levels was detected by Western blot analysis and RT-PCR. The concentration of prostaglandin E2 (PGE2) and Cytokines in the culture supernatant of neutrophils was determined using ELISA. Superoxide generation was measured by the cytochrome c reduction method. Elastase activity was measured using a chromogenic substrate assay specific for human neutrophil elastase. FMLP and OZ enhanced PGE2 Release through induction of COX-2 protein and mRNA expression. FMLP- or OZ-induced PGE2 Release was abolished by the addition of NS-398 or nimesulide; nevertheless, even a high concentration of COX-2 inhibitor did not change FMLP- or OZ-induced expression of COX-2 at message and protein levels. Although FMLP- or OZ-induced superoxide generation and elastase Release were not affected by the addition of COX-2 inhibitor, Cytokine Release such as interleukin (IL)-1beta, IL-6 and IL-8 was significantly inhibited by high concentration of COX-2 inhibitor, but tumor necrosis factor-alpha (TNF-alpha) was partially attenuated. These studies showed that selective COX-2 inhibitors, NS-398 and nimesulide, suppressed PGE2 and proinflammatory Cytokine Release in activated neutrophils. These results suggest that selective COX-2 inhibitors may contribute to resolution of acute inflammation through the reduction of inflammatory Cytokine Release in activated neutrophils.
