Brazilian Journal of Pulmonology

ISSN (on-line): 1806-3756 | ISSN (printed): 1806-3713

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Aminoguanidine reduces oxidative stress and structural lung changes in experimental diabetes mellitus

Aminoguanidina reduz o estresse oxidativo e as alterações estruturais pulmonares em diabetes mellitus experimental

Fabio Cangeri Di Naso, Luiz Alberto Forgiarini Junior, Luiz Felipe Forgiarini, Marilene Porawski, Alexandre Simões Dias, Norma Anair Possa Marroni

J Bras Pneumol.2010;36(4):-

Abstract PDF PT PDF EN Portuguese Text

We evaluated the effect of aminoguanidine on pulmonary oxidative stress and lung structure in an experimental model of diabetes mellitus. Thiobarbituric acid reactive substances (TBARS), histology and arterial blood gases were evaluated in animals with diabetes mellitus (DM group), animals with diabetes mellitus treated with aminoguanidine (DM+AG group), and controls. The TBARS levels were significantly higher in the DM group than in the control and DM+AG groups (2.90 ± 1.12 vs. 1.62 ± 0.28 and 1.68 ± 0.04 nmol/mg protein, respectively), as was PaCO2 when compared with that of the control group (49.2 ± 1.65 vs. 38.12 ± 4.85 mmHg), and PaO2 was significantly higher in the control group (104.5 ± 6.3 vs. 16.30 ± 69.48 and 97.05±14.02 mmHg, respectively). In this experimental model of diabetes mellitus, aminoguanidine reduced oxidative stress, structural tissue alterations, and gas exchange.

 


Keywords: Oxidative stress; Diabetes mellitus, experimental; Lung.

 


Effects of methylprednisolone on inflammatory activity and oxidative stress in the lungs of brain-dead rats

Efeitos da metilprednisolona na atividade inflamatória e estresse oxidativo nos pulmões de ratoscom morte cerebral

Eduardo Sperb Pilla, Raôni Bins Pereira, Luiz Alberto Forgiarini Junior, Luiz Felipe Forgiarini,Artur de Oliveira Paludo, Jane Maria Ulbrich Kulczynski, Paulo Francisco Guerreiro Cardoso,Cristiano Feijó Andrade

J Bras Pneumol.2013;39(2):173-180

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Objective: To evaluate the effects that early and late systemic administration of methylprednisolone have on lungs in a rat model of brain death. Methods: Twenty-four male Wistar rats were anesthetized and randomly divided into four groups (n = 6 per group): sham-operated (sham); brain death only (BD); brain death plus methylprednisolone (30 mg/kg i.v.) after 5 min (MP5); and brain death plus methylprednisolone (30 mg/kg i.v.) after 60 min (MP60). In the BD, MP5, and MP60 group rats, we induced brain death by inflating a balloon catheter in the extradural space. All of the animals were observed and ventilated for 120 min. We determined hemodynamic and arterial blood gas variables; wet/dry weight ratio; histological score; levels of thiobarbituric acid reactive substances (TBARS); superoxide dismutase (SOD) activity; and catalase activity. In BAL fluid, we determined differential white cell counts, total protein, and lactate dehydrogenase levels. Myeloperoxidase activity, lipid peroxidation, and TNF-α levels were assessed in lung tissue. Results: No significant differences were found among the groups in terms of hemodynamics, arterial blood gases, wet/dry weight ratio, BAL fluid analysis, or histological score-nor in terms of SOD, myeloperoxidase, and catalase activity. The levels of TBARS were significantly higher in the MP5 and MP60 groups than in the sham and BD groups (p < 0.001). The levels of TNF-α were significantly lower in the MP5 and MP60 groups than in the BD group (p < 0.001). Conclusions:áIn this model of brain death, the early and late administration of methylprednisolone had similar effects on inflammatory activity and lipid peroxidation in lung tissue.

 


Palavras-chave: Ratos; Morte encefálica; Estresse oxidativo; Pulmão; Hidroxicorticosteroides.

 


Uncoupling protein-2 mRNA expression in mice subjected to intermittent hypoxia

Expressão do mRNA da uncoupling protein-2 em camundongos submetidos à hipóxia intermitente

Luciana Rodrigues Vieira, Denis Martinez, Luiz Felipe Forgiarini, Darlan Pase da Rosa, Gustavo Alfredo Ochs de Muñoz, Micheli Fagundes, Emerson Ferreira Martins, Carolina Caruccio Montanari, Cintia Zappe Fiori

J Bras Pneumol.2015;41(2):167-174

Abstract PDF PT PDF EN Portuguese Text

Objective: To investigate the effect of intermittent hypoxia-a model of obstructive sleep apnea (OSA)-on pancreatic expression of uncoupling protein-2 (UCP2), as well as on glycemic and lipid profiles, in C57BL mice. Methods: For 8 h/day over a 35-day period, male C57BL mice were exposed to intermittent hypoxia (hypoxia group) or to a sham procedure (normoxia group). The intermittent hypoxia condition involved exposing mice to an atmosphere of 92% N and 8% CO2 for 30 s, progressively reducing the fraction of inspired oxygen to 8 ± 1%, after which they were exposed to room air for 30 s and the cycle was repeated (480 cycles over the 8-h experimental period). Pancreases were dissected to isolate the islets. Real-time PCR was performed with TaqMan assays. Results: Expression of UCP2 mRNA in pancreatic islets was 20% higher in the normoxia group than in the hypoxia group (p = 0.11). Fasting serum insulin was higher in the hypoxia group than in the normoxia group (p = 0.01). The homeostasis model assessment of insulin resistance indicated that, in comparison with the control mice, the mice exposed to intermittent hypoxia showed 15% lower insulin resistance (p = 0.09) and 21% higher pancreatic β-cell function (p = 0.01). Immunohistochemical staining of the islets showed no significant differences between the two groups in terms of the area or intensity of α- and β-cell staining for insulin and glucagon. Conclusions: To our knowledge, this is the first report of the effect of intermittent hypoxia on UCP2 expression. Our findings suggest that UCP2 regulates insulin production in OSA. Further study of the role that UCP2 plays in the glycemic control of OSA patients is warranted.

 


Keywords: Blood glucose; Sleep apnea syndromes; Pancreas; Glucagon-secreting cells.

 


 

 


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