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1

Effect of exogenous pulmonary surfactant preparations on the structure of pulmonary alveoli in newborn rats

100%
Zurawski J., Wasowicz M., Marszalek A., Florek E., Biczysko W.
Folia Histochemica et Cytobiologica
|
2002
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tom 40
|
nr 3
2

GM-CSF regulation in eosinophils

84%
Esnault S., Malter J. S.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
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tom 50
|
nr 2
3
Content available remote

Beneficial effect of alpha-lipoic acid on lipopolysaccharide-induced oxidative stress in bronchoalveolar lavage fluid

84%
Goraca A., Skibska B.
Journal of Physiology and Pharmacology
|
2008
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tom 59
|
nr 2
Lipopolysaccharide (LPS) from gram-negative bacteria is a major factor that contributes to multiple organ failure including lung injury. Among LPS-induced metabolites, reactive oxygen species are considered to play a crucial pathogenic role in the lung damage. In this study, the effect of early administration of an antioxidant, a-lipoic acid (LA), on bronchoalveoar lavage fluid (BALF) lipid peroxidation, hydrogen peroxide (H2O2), sulphydryl group (-SH) concentration and total protein concentration was evaluated in rats with endotoxic shock induced by administration of LPS (Escherichia coli 026:B6, 30 mg/kg, i.v.). The animals were treated intravenously with normal saline or LA (60 mg/kg or 100 mg/kg i.v.) 30 min after LPS injection. Five hours after LPS or saline administration, the animals were sacrificed and BALF was obtained for measurements. The results showed that the levels of oxidative markers, thiobarbituric acid reactive substances (TBARS) and H2O2 were increased significantly in BALF, whereas they were decreased significantly on treatment with LA. The concentrations of -SH groups were significantly increased and total protein concentration was insignificantly decreased in the LPS/LA group. There was no difference in oxidative stress reduction between 60 mg/kg and 100 mg/kg doses. These results indicate that early administration of lipoic acid provides protective effects against endotoxin-induced oxidative stress in the lung and supports the idea that alpha-lipoic acid is a free radical scavenger and a potent antioxidant.
4
Content available remote

Bradykinin in ischemia-reperfusion injury of the rat lung

67%
Nowak K., Weih S., Post S., Gebhard M. M., Hohenberger P.
Journal of Physiology and Pharmacology. Supplement
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2007
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tom 58
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nr 5
5
Content available remote

A low vitamin A status increases the susceptibility to cigarette smoke-induced lung emphysema in C57BL/6J mice

67%
Van Eijl S., Mortaz E., Versluis C., Nijkamp F. P., Folkerts G., Bloksma N.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 2
Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. Cigarette smoke has been considered a major player in the pathogenesis of COPD. The inflamed airways of COPD patients contain several inflammatory cells. Vitamin A metabolites have been implicated in the repair of lung damage. Exposure to cigarette smoke has been shown to depress levels of retinol in lungs of rats. The purpose of this study was to investigate if a low, but not deficient, vitamin A status potentiated susceptibility to the development of cigarette smoke-induced lung emphysema in mice. Mice were bred that were the offspring’s of 3 generations of mice that were fed a purified diet containing low levels of vitamin A and exposed to cigarette smoke for 3 months, every weekday. Then, levels of 9-cis, 13-cis, and all-trans retinoic acid, retinol and retinyl palmitate were measured in plasma, liver and right lung lobe. The left lung lobe was used to assess mean linear intercept (Lm), as a measure of smoke-induced lung damage. Average feed intakes were not different between treatment groups. We show that both retinol and retinyl palmitate levels were dramatically decreased in the storage organs of mice on the low vitamin A diet (retinol 2-fold in both lung and liver, and retinyl palmitate 5- fold in lung) which shows that the depletion was successful. However, this treatment did not result in the development of lung emphysema. However, smoke exposure led to a significant increase in Lm in mice with a low vitamin A status compared to the room air-breathing controls. Lung levels of acid retinoids were similar in all mice, irrespective of diet or smoke exposure. Concluding, a low vitamin A status increases the susceptibility to the development of cigarette smoke-induced lung emphysema, possibly because of decreased anti-oxidant capacity in the lungs due to locally reduced retinol and retinyl palmitate levels. These observations indicate that human populations with a low vitamin A status and a high prevalence of smoking may be at increased risk of developing lung emphysema.
6

Spojrzenie polskiego lekarza weterynarii

59%
Niziolek R.
Weterynaria po Dyplomie
|
2020
|
tom 21
|
nr 5
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