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Pituitary Adenylate Cyclase-Activating Polypeptide Reverses Ammonium Metavanadate-Induced Airway Hyperresponsiveness in Rats.

Tlili M, Rouatbi S, Sriha B, Ben Rhouma K, Sakly M, Vaudry D, Wurtz O, Tebourbi O - Oxid Med Cell Longev (2015)

Bottom Line: Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration.PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1α and TNF-α) in alveolar macrophages and improved the antioxidant status.PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Integrated Physiology, Science Faculty of Bizerte, Carthage University, 7021 Zarzouna, Tunisia ; National Institute of Health and Medical Research (INSERM), U982, 76821 Mont-Saint-Aignan Cedex, France ; Institute for Research and Innovation in Biomedicine (IRIB), Normandy University, 76821 Mont-Saint-Aignan Cedex, France ; Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Rouen University, 76821 Mont-Saint-Aignan Cedex, France.

ABSTRACT
The rate of atmospheric vanadium is constantly increasing due to fossil fuel combustion. This environmental pollution favours vanadium exposure in particular to its vanadate form, causing occupational bronchial asthma and bronchitis. Based on the well admitted bronchodilator properties of the pituitary adenylate cyclase-activating polypeptide (PACAP), we investigated the ability of this neuropeptide to reverse the vanadate-induced airway hyperresponsiveness in rats. Exposure to ammonium metavanadate aerosols (5 mg/m(3)/h) for 15 minutes induced 4 hours later an array of pathophysiological events, including increase of bronchial resistance and histological alterations, activation of proinflammatory alveolar macrophages, and increased oxidative stress status. Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration. PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1α and TNF-α) in alveolar macrophages and improved the antioxidant status. PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal. Then, the development of stable analogs of PACAP could represent a promising therapeutic alternative for the treatment of inflammatory respiratory disorders.

No MeSH data available.


Related in: MedlinePlus

Inhalation of PACAP aerosols inhibits AMV-dependent increase of lung resistance. Rats received aerosols of AMV (5 mg/m3/h) for 15 minutes followed or not by PACAP aerosols (P38, 0.1 mM) for 10 minutes. Control rats inhaled vehicle (Veh.) only. Values are expressed as means ± SEM (n = 8 for each experimental group). ∗∗p < 0.01 based on one-way ANOVA followed by Tukey's multiple comparison post hoc test.
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fig2: Inhalation of PACAP aerosols inhibits AMV-dependent increase of lung resistance. Rats received aerosols of AMV (5 mg/m3/h) for 15 minutes followed or not by PACAP aerosols (P38, 0.1 mM) for 10 minutes. Control rats inhaled vehicle (Veh.) only. Values are expressed as means ± SEM (n = 8 for each experimental group). ∗∗p < 0.01 based on one-way ANOVA followed by Tukey's multiple comparison post hoc test.

Mentions: As indicated by the dose response experiment, a significant increase of lung resistance was observed in rats exposed to vanadium for 15 minutes compared to animals treated with vehicle aerosols only (2.53 ± 0.05 versus 0.45 ± 0.02 KPa/L/s in control animals, p < 0.01; Figure 2). When AMV-sensitized rats were exposed to PACAP aerosols (0.1 mM) for 10 additional minutes, the increase of LR was totally reversed to a level similar to that of the control animals (0.61 ± 0.03 KPa/L/s; Figure 2).


Pituitary Adenylate Cyclase-Activating Polypeptide Reverses Ammonium Metavanadate-Induced Airway Hyperresponsiveness in Rats.

Tlili M, Rouatbi S, Sriha B, Ben Rhouma K, Sakly M, Vaudry D, Wurtz O, Tebourbi O - Oxid Med Cell Longev (2015)

Inhalation of PACAP aerosols inhibits AMV-dependent increase of lung resistance. Rats received aerosols of AMV (5 mg/m3/h) for 15 minutes followed or not by PACAP aerosols (P38, 0.1 mM) for 10 minutes. Control rats inhaled vehicle (Veh.) only. Values are expressed as means ± SEM (n = 8 for each experimental group). ∗∗p < 0.01 based on one-way ANOVA followed by Tukey's multiple comparison post hoc test.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4496651&req=5

fig2: Inhalation of PACAP aerosols inhibits AMV-dependent increase of lung resistance. Rats received aerosols of AMV (5 mg/m3/h) for 15 minutes followed or not by PACAP aerosols (P38, 0.1 mM) for 10 minutes. Control rats inhaled vehicle (Veh.) only. Values are expressed as means ± SEM (n = 8 for each experimental group). ∗∗p < 0.01 based on one-way ANOVA followed by Tukey's multiple comparison post hoc test.
Mentions: As indicated by the dose response experiment, a significant increase of lung resistance was observed in rats exposed to vanadium for 15 minutes compared to animals treated with vehicle aerosols only (2.53 ± 0.05 versus 0.45 ± 0.02 KPa/L/s in control animals, p < 0.01; Figure 2). When AMV-sensitized rats were exposed to PACAP aerosols (0.1 mM) for 10 additional minutes, the increase of LR was totally reversed to a level similar to that of the control animals (0.61 ± 0.03 KPa/L/s; Figure 2).

Bottom Line: Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration.PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1α and TNF-α) in alveolar macrophages and improved the antioxidant status.PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Integrated Physiology, Science Faculty of Bizerte, Carthage University, 7021 Zarzouna, Tunisia ; National Institute of Health and Medical Research (INSERM), U982, 76821 Mont-Saint-Aignan Cedex, France ; Institute for Research and Innovation in Biomedicine (IRIB), Normandy University, 76821 Mont-Saint-Aignan Cedex, France ; Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Rouen University, 76821 Mont-Saint-Aignan Cedex, France.

ABSTRACT
The rate of atmospheric vanadium is constantly increasing due to fossil fuel combustion. This environmental pollution favours vanadium exposure in particular to its vanadate form, causing occupational bronchial asthma and bronchitis. Based on the well admitted bronchodilator properties of the pituitary adenylate cyclase-activating polypeptide (PACAP), we investigated the ability of this neuropeptide to reverse the vanadate-induced airway hyperresponsiveness in rats. Exposure to ammonium metavanadate aerosols (5 mg/m(3)/h) for 15 minutes induced 4 hours later an array of pathophysiological events, including increase of bronchial resistance and histological alterations, activation of proinflammatory alveolar macrophages, and increased oxidative stress status. Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration. PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1α and TNF-α) in alveolar macrophages and improved the antioxidant status. PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal. Then, the development of stable analogs of PACAP could represent a promising therapeutic alternative for the treatment of inflammatory respiratory disorders.

No MeSH data available.


Related in: MedlinePlus