The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Bo Zhang - One of the best experts on this subject based on the ideXlab platform.
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Simulated Aeromedical Evacuation Exacerbates Burn Induced Lung Injury: Targeting Mitochondrial DNA for Reversal
2020Co-Authors: Mengjing Xiao, Xiaofang Zou, Bo ZhangAbstract:Abstract Background: Aeromedical evacuation of patients with Burn trauma is an important transport method at both wartime and peacetime, which exposes patients to prolonged periods of hypobaric hypoxia. However, the effects of such exposure on Burn injury, particularly on Burn induced Lung injury are largely unexplored. The objective of this study is to investigate the effect of hypobaric hypoxia on Burn induced Lung injury and to discuss the possible mechanism by using a rat Burn model. Methods: Male wistar rats inflicted with 30% total body surface area Burn were exposed to hypobaric hypoxia condition (simulated 2000m altitude) or normoxia control for 24 h. Deoxyribonuclease I was systemically administrated as treatment intervention. Systemic inflammatory mediators and mitochondrial deoxyribonucleic acid level were detected. The histopathological examination, and acute Lung injury score were determined. Malonaldehyde content, myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome level in the Lung tissue were measured. Data among groups were compared by using analysis of variance followed by the post hoc analysis of Tukey's test. Results: Burn resulted in remarkably higher level of systemic inflammatory cytokines and mitochondrial deoxyribonucleic acid release, which was further heightened by hypobaric hypoxia exposure. Moreover, hypobaric hypoxia exposure gave rise to increased NLRP3 inflammasome expression, elevated malonaldehyde content and myeloperoxidase activity in the Lung. Burn induced Lung injury was exacerbated as shown by histopathological examination and acute Lung injury score. Administration of deoxyribonuclease I markedly reduced mitochondrial deoxyribonucleic acid release and systemic inflammatory cytokines production. Furthermore, NLRP3 inflammasome level in the Lung tissue was decreased and Burn induced Lung injury was ameliorated. Conclusions: Our results suggested that simulated aeromedical evacuation further increased the Burn induced mitochondrial deoxyribonucleic acid release and exacerbated Burn induced inflammation and Lung injury. Deoxyribonuclease I reduced the release of mitochondrial deoxyribonucleic acid and limited the mitochondrial deoxyribonucleic acid-induced systemic inflammation, ameliorated Burn-induced acute Lung injury. Intervening mitochondrial deoxyribonucleic acid level could be a potential target to protect from Burn-induced Lung injury during aeromedical conditions and provide with safer air evacuations for severely Burned patients.
Mengjing Xiao - One of the best experts on this subject based on the ideXlab platform.
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Simulated Aeromedical Evacuation Exacerbates Burn Induced Lung Injury: Targeting Mitochondrial DNA for Reversal
2020Co-Authors: Mengjing Xiao, Xiaofang Zou, Bo ZhangAbstract:Abstract Background: Aeromedical evacuation of patients with Burn trauma is an important transport method at both wartime and peacetime, which exposes patients to prolonged periods of hypobaric hypoxia. However, the effects of such exposure on Burn injury, particularly on Burn induced Lung injury are largely unexplored. The objective of this study is to investigate the effect of hypobaric hypoxia on Burn induced Lung injury and to discuss the possible mechanism by using a rat Burn model. Methods: Male wistar rats inflicted with 30% total body surface area Burn were exposed to hypobaric hypoxia condition (simulated 2000m altitude) or normoxia control for 24 h. Deoxyribonuclease I was systemically administrated as treatment intervention. Systemic inflammatory mediators and mitochondrial deoxyribonucleic acid level were detected. The histopathological examination, and acute Lung injury score were determined. Malonaldehyde content, myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome level in the Lung tissue were measured. Data among groups were compared by using analysis of variance followed by the post hoc analysis of Tukey's test. Results: Burn resulted in remarkably higher level of systemic inflammatory cytokines and mitochondrial deoxyribonucleic acid release, which was further heightened by hypobaric hypoxia exposure. Moreover, hypobaric hypoxia exposure gave rise to increased NLRP3 inflammasome expression, elevated malonaldehyde content and myeloperoxidase activity in the Lung. Burn induced Lung injury was exacerbated as shown by histopathological examination and acute Lung injury score. Administration of deoxyribonuclease I markedly reduced mitochondrial deoxyribonucleic acid release and systemic inflammatory cytokines production. Furthermore, NLRP3 inflammasome level in the Lung tissue was decreased and Burn induced Lung injury was ameliorated. Conclusions: Our results suggested that simulated aeromedical evacuation further increased the Burn induced mitochondrial deoxyribonucleic acid release and exacerbated Burn induced inflammation and Lung injury. Deoxyribonuclease I reduced the release of mitochondrial deoxyribonucleic acid and limited the mitochondrial deoxyribonucleic acid-induced systemic inflammation, ameliorated Burn-induced acute Lung injury. Intervening mitochondrial deoxyribonucleic acid level could be a potential target to protect from Burn-induced Lung injury during aeromedical conditions and provide with safer air evacuations for severely Burned patients.
Xiaofang Zou - One of the best experts on this subject based on the ideXlab platform.
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Simulated Aeromedical Evacuation Exacerbates Burn Induced Lung Injury: Targeting Mitochondrial DNA for Reversal
2020Co-Authors: Mengjing Xiao, Xiaofang Zou, Bo ZhangAbstract:Abstract Background: Aeromedical evacuation of patients with Burn trauma is an important transport method at both wartime and peacetime, which exposes patients to prolonged periods of hypobaric hypoxia. However, the effects of such exposure on Burn injury, particularly on Burn induced Lung injury are largely unexplored. The objective of this study is to investigate the effect of hypobaric hypoxia on Burn induced Lung injury and to discuss the possible mechanism by using a rat Burn model. Methods: Male wistar rats inflicted with 30% total body surface area Burn were exposed to hypobaric hypoxia condition (simulated 2000m altitude) or normoxia control for 24 h. Deoxyribonuclease I was systemically administrated as treatment intervention. Systemic inflammatory mediators and mitochondrial deoxyribonucleic acid level were detected. The histopathological examination, and acute Lung injury score were determined. Malonaldehyde content, myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome level in the Lung tissue were measured. Data among groups were compared by using analysis of variance followed by the post hoc analysis of Tukey's test. Results: Burn resulted in remarkably higher level of systemic inflammatory cytokines and mitochondrial deoxyribonucleic acid release, which was further heightened by hypobaric hypoxia exposure. Moreover, hypobaric hypoxia exposure gave rise to increased NLRP3 inflammasome expression, elevated malonaldehyde content and myeloperoxidase activity in the Lung. Burn induced Lung injury was exacerbated as shown by histopathological examination and acute Lung injury score. Administration of deoxyribonuclease I markedly reduced mitochondrial deoxyribonucleic acid release and systemic inflammatory cytokines production. Furthermore, NLRP3 inflammasome level in the Lung tissue was decreased and Burn induced Lung injury was ameliorated. Conclusions: Our results suggested that simulated aeromedical evacuation further increased the Burn induced mitochondrial deoxyribonucleic acid release and exacerbated Burn induced inflammation and Lung injury. Deoxyribonuclease I reduced the release of mitochondrial deoxyribonucleic acid and limited the mitochondrial deoxyribonucleic acid-induced systemic inflammation, ameliorated Burn-induced acute Lung injury. Intervening mitochondrial deoxyribonucleic acid level could be a potential target to protect from Burn-induced Lung injury during aeromedical conditions and provide with safer air evacuations for severely Burned patients.
B.Ç. Yeğen - One of the best experts on this subject based on the ideXlab platform.
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Estrogens ameliorate remote organ inflammation induced by Burn injury in rats
Inflammation Research, 2001Co-Authors: E.s. Özveri, A. Bozkurt, G. Haklar, Ş. Çetinel, S. Arbak, C. Yeğen, B.Ç. YeğenAbstract:Objective and design: The present study was designed to investigate the role of sex steroids in Burn-induced remote organ injury.¶ Material or subjects: Male Wistar albino rats were given Burn trauma (n=39) , and underwent castration or sham operation at 2 h following the Burn injury.¶ Treatment: Rats were injected sc with either 17 β estradiol benzoate (E_2, 10 mg/kg) or an androgen receptor blocker cyproterone acetate (CPA, 25 mg/kg) or vehicle, immediately after Burn and at 12 h.¶ Methods: At 24 h of Burn insult, rats were decapitated. Blood samples for RIA of testosterone, estradiol and tumor necrosis factor (TNF)- α and the tissue samples for myeloperoxidase activitiy (MPO) were taken. ANOVA student's t test was used for statistical analysis.¶ Results: Castration, antiandrogen and E_2 treatments increased plasma estradiol levels and depressed Burn-induced elevation in serum TNF- α levels. In the liver and Lung, Burn-induced increase in MPO was reduced by E_2 and castration, while CPA was effective in reducing neutrophil infiltration only in the liver.¶ Conclusion: We propose that treatment with estrogens or antiandrogens might be applicable in clinical situations to ameliorate systemic inflammation induced by Burn.
E.s. Özveri - One of the best experts on this subject based on the ideXlab platform.
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Estrogens ameliorate remote organ inflammation induced by Burn injury in rats
Inflammation Research, 2001Co-Authors: E.s. Özveri, A. Bozkurt, G. Haklar, Ş. Çetinel, S. Arbak, C. Yeğen, B.Ç. YeğenAbstract:Objective and design: The present study was designed to investigate the role of sex steroids in Burn-induced remote organ injury.¶ Material or subjects: Male Wistar albino rats were given Burn trauma (n=39) , and underwent castration or sham operation at 2 h following the Burn injury.¶ Treatment: Rats were injected sc with either 17 β estradiol benzoate (E_2, 10 mg/kg) or an androgen receptor blocker cyproterone acetate (CPA, 25 mg/kg) or vehicle, immediately after Burn and at 12 h.¶ Methods: At 24 h of Burn insult, rats were decapitated. Blood samples for RIA of testosterone, estradiol and tumor necrosis factor (TNF)- α and the tissue samples for myeloperoxidase activitiy (MPO) were taken. ANOVA student's t test was used for statistical analysis.¶ Results: Castration, antiandrogen and E_2 treatments increased plasma estradiol levels and depressed Burn-induced elevation in serum TNF- α levels. In the liver and Lung, Burn-induced increase in MPO was reduced by E_2 and castration, while CPA was effective in reducing neutrophil infiltration only in the liver.¶ Conclusion: We propose that treatment with estrogens or antiandrogens might be applicable in clinical situations to ameliorate systemic inflammation induced by Burn.
