Therapeutic effect of recombinant human catalase on H1N1 influenza-induced pneumonia in mice.
Identifieur interne : 001750 ( Main/Curation ); précédent : 001749; suivant : 001751Therapeutic effect of recombinant human catalase on H1N1 influenza-induced pneumonia in mice.
Auteurs : Xun-Long Shi [République populaire de Chine] ; Zhi-Hui Shi ; Hai Huang ; Hong-Guang Zhu ; Pei Zhou ; Dianwen JuSource :
- Inflammation [ 1573-2576 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Antioxydants (pharmacologie), Catalase (pharmacologie), Estimation de Kaplan-Meier, Femelle, Humains, Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (mortalité), Infections à Orthomyxoviridae (traitement médicamenteux), Lignées consanguines de souris, Pneumopathie virale (anatomopathologie), Pneumopathie virale (mortalité), Pneumopathie virale (traitement médicamenteux), Poumon (anatomopathologie), Poumon (métabolisme), Protéines recombinantes (pharmacologie), Radical hydroxyle (métabolisme), Souris, Sous-type H1N1 du virus de la grippe A, Stress oxydatif (), Superoxydes (métabolisme).
- MESH :
- anatomopathologie : Infections à Orthomyxoviridae, Pneumopathie virale, Poumon.
- mortalité : Infections à Orthomyxoviridae, Pneumopathie virale.
- métabolisme : Poumon, Radical hydroxyle, Superoxydes.
- pharmacologie : Antioxydants, Catalase, Protéines recombinantes.
- traitement médicamenteux : Infections à Orthomyxoviridae, Pneumopathie virale.
- Animaux, Estimation de Kaplan-Meier, Femelle, Humains, Lignées consanguines de souris, Souris, Sous-type H1N1 du virus de la grippe A, Stress oxydatif.
English descriptors
- KwdEn :
- Animals, Antioxidants (pharmacology), Catalase (pharmacology), Female, Humans, Hydroxyl Radical (metabolism), Influenza A Virus, H1N1 Subtype, Kaplan-Meier Estimate, Lung (metabolism), Lung (pathology), Mice, Mice, Inbred Strains, Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (mortality), Orthomyxoviridae Infections (pathology), Oxidative Stress (drug effects), Pneumonia, Viral (drug therapy), Pneumonia, Viral (mortality), Pneumonia, Viral (pathology), Recombinant Proteins (pharmacology), Superoxides (metabolism).
- MESH :
- chemical , metabolism : Hydroxyl Radical, Superoxides.
- chemical , pharmacology : Antioxidants, Catalase, Recombinant Proteins.
- drug effects : Oxidative Stress.
- drug therapy : Orthomyxoviridae Infections, Pneumonia, Viral.
- metabolism : Lung.
- mortality : Orthomyxoviridae Infections, Pneumonia, Viral.
- pathology : Lung, Orthomyxoviridae Infections, Pneumonia, Viral.
- Animals, Female, Humans, Influenza A Virus, H1N1 Subtype, Kaplan-Meier Estimate, Mice, Mice, Inbred Strains.
Abstract
Reactive oxygen species (ROS) are believed to play a key role in the induction of lung damage caused by pneumonia and therapeutic agents that could effectively scavenge ROS may prevent or reduce the deleterious effects of influenza-induced pneumonia. In this study, we first demonstrated that human catalase could attenuate acute oxidative injury in lung tissues following influenza-induced pneumonia. Mice were infected with influenza virus H1N1 (FM1 strain) and treated with recombinant human catalase (50,000 U/kg) by inhalation. The survival time and survival rates of H1N1 induced pneumonia mice were increased by treatment with recombinant human catalase. Protective efficacy of catalase was also observed in lung histology, anti-oxidant parameters, pulmonary pathology and influenza viral titer in lungs in mice. These observations were associated with increased serum superoxide and hydroxyl radical anion scavenging capacities. This study strongly indicated that recombinant catalase might be a potential therapy for H1N1 influenza-induced pneumonia.
DOI: 10.1007/s10753-009-9170-y
PubMed: 19957025
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pubmed:19957025Le document en format XML
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<term>Humans</term>
<term>Hydroxyl Radical (metabolism)</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Kaplan-Meier Estimate</term>
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<front><div type="abstract" xml:lang="en">Reactive oxygen species (ROS) are believed to play a key role in the induction of lung damage caused by pneumonia and therapeutic agents that could effectively scavenge ROS may prevent or reduce the deleterious effects of influenza-induced pneumonia. In this study, we first demonstrated that human catalase could attenuate acute oxidative injury in lung tissues following influenza-induced pneumonia. Mice were infected with influenza virus H1N1 (FM1 strain) and treated with recombinant human catalase (50,000 U/kg) by inhalation. The survival time and survival rates of H1N1 induced pneumonia mice were increased by treatment with recombinant human catalase. Protective efficacy of catalase was also observed in lung histology, anti-oxidant parameters, pulmonary pathology and influenza viral titer in lungs in mice. These observations were associated with increased serum superoxide and hydroxyl radical anion scavenging capacities. This study strongly indicated that recombinant catalase might be a potential therapy for H1N1 influenza-induced pneumonia.</div>
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