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. 2013:2013:549879.
doi: 10.1155/2013/549879. Epub 2013 Feb 27.

Anacardic acids from cashew nuts ameliorate lung damage induced by exposure to diesel exhaust particles in mice

Ana Laura Nicoletti Carvalho  1 , Raquel Annoni, Larissa Helena Lobo Torres, Ana Carolina Cardoso Santos Durão, Ana Lucia Borges Shimada, Francine Maria Almeida, Cristina Bichels Hebeda, Fernanda Degobbi Tenorio Quirino Santos Lopes, Marisa Dolhnikoff, Milton Arruda Martins, Luiz Fernando Ferraz Silva, Sandra Helena Poliselli Farsky, Paulo Hilário Nascimento Saldiva, Cornelia M Ulrich, Robert W Owen, Tania Marcourakis, Maria Teresa Salles Trevisan, Thais Mauad
Affiliations

Anacardic acids from cashew nuts ameliorate lung damage induced by exposure to diesel exhaust particles in mice

Ana Laura Nicoletti Carvalho et al. Evid Based Complement Alternat Med. 2013.

Abstract

Anacardic acids from cashew nut shell liquid, a Brazilian natural substance, have antimicrobial and antioxidant activities and modulate immune responses and angiogenesis. As inflammatory lung diseases have been correlated to environmental pollutants exposure and no reports addressing the effects of dietary supplementation with anacardic acids on lung inflammation in vivo have been evidenced, we investigated the effects of supplementation with anacardic acids in a model of diesel exhaust particle- (DEP-) induced lung inflammation. BALB/c mice received an intranasal instillation of 50 μ g of DEP for 20 days. Ten days prior to DEP instillation, animals were pretreated orally with 50, 150, or 250 mg/kg of anacardic acids or vehicle (100 μ L of cashew nut oil) for 30 days. The biomarkers of inflammatory and antioxidant responses in the alveolar parenchyma, bronchoalveolar lavage fluid (BALF), and pulmonary vessels were investigated. All doses of anacardic acids ameliorated antioxidant enzyme activities and decreased vascular adhesion molecule in vessels. Animals that received 50 mg/kg of anacardic acids showed decreased levels of neutrophils and tumor necrosis factor in the lungs and BALF, respectively. In summary, we demonstrated that AAs supplementation has a potential protective role on oxidative and inflammatory mechanisms in the lungs.

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Figures

Figure 1
Figure 1
Chemical structure of anacardic acids.
Figure 2
Figure 2
Glutathione reductase (a), glutathione peroxidase (b), glutathione S-transferase (c), and catalase (d) activities in lungs. Values represent means ± SEM. Ctrl: control; animals received an intranasal instillation of 10 μL saline solution and were treated orally with 100 μL of cashew nut oil (CNO). DEP: diesel exhaust particles; intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 100 μL of CNO. DA50: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 50 mg/kg of AAs. DA150: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 150 mg/kg of AAs. DA250: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 250 mg/kg of AAs. # P < 0.05 relative to Ctrl. *P < 0.05 relative to DEP. ## P < 0.001 relative to Ctrl. **P < 0.001 relative to DEP.
Figure 3
Figure 3
Glutathione reductase (a), glutathione peroxidase (b), glutathione S-transferase (c), and catalase (d) activities in blood. Values represent means ± SEM. Ctrl: control; animals received an intranasal instillation of 10 μL saline solution and were treated orally with 100 μL of cashew nut oil (CNO). DEP: diesel exhaust particles; intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 100 μL of CNO. DA50: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 50 mg/kg of AAs. DA150: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 150 mg/kg of AAs. DA250: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 250 mg/kg of AAs. # P < 0.05 relative to Ctrl.
Figure 4
Figure 4
Photomicrographs showing a panoramic view of the inflammatory response in the lung tissue caused by DEP. The DEP group (b) demonstrated increased inflammatory response compared with the Ctrl group in the alveolar parenchyma (a). In detail (c), diesel particles phagocytized by a macrophage in the lung of an animal treated with DEP for 20 days. A black spot of anthracotic pigment can be observed in the inset (H&E). Scale bars = 25 μm.
Figure 5
Figure 5
Photomicrographs showing the neutrophil density in lung tissue. The DEP group (b) demonstrated increased neutrophil density (in detail, the arrows are indicating some neutrophils) compared with the Ctrl group (a). Oral supplementation with 50 and 150 mg/kg of AAs was able to reduce the influx of neutrophils in lung tissue (c and d, resp.) (H&E). Scale bars = 25 μm.
Figure 6
Figure 6
Influx of neutrophils (a) and macrophages (b) in the alveolar parenchyma. Values represent means ± SEM. Ctrl: control; animals received an intranasal instillation of 10 μL saline solution and were treated orally with 100 μL of cashew nut oil (CNO). DEP: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 100 μL of CNO. DA50: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 50 mg/kg of AAs. DA150: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 150 mg/kg of AAs. DA250: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 250 mg/kg of AAs. # P < 0.001 relative to Ctrl. *P < 0.05 relative to DEP.
Figure 7
Figure 7
8-isoprostane (a), KC (b), TNF-α (c) and NF-κB (d) in the alveolar parenchyma. Values represent means ± SEM or medians (interquartile range). Ctrl: control; animals received an intranasal instillation of 10 μL saline solution and were treated orally with 100 μL of cashew nut oil (CNO). DEP: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 100 μL of CNO. DA50: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 50 mg/kg of AAs. DA150: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 150 mg/kg of AAs. DA250: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 250 mg/kg of AAs. KC: keratinocyte chemoattractant. TNF-α: tumor necrosis factor-alpha. NF-κB: nuclear factor-kappa B. # P < 0.001 relative to Ctrl.  *P < 0.05 relative to DEP.
Figure 8
Figure 8
Vascular adhesion molecule (VCAM) (a) and KC (b) positive areas in peribronchiolar vessels. Values represent means ± SEM. Ctrl: control; animals received an intranasal instillation of 10 μL saline solution and were treated orally with 100 μL of cashew nut oil (CNO). DEP: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 100 μL of CNO. DA50: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 50 mg/kg of AAs. DA150: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 150 mg/kg of AAs. DA250: intranasal instillation of 50 μg DEP/10 μL of saline and treated orally with 250 mg/kg of AAs. KC: keratinocyte chemoattractant. # P < 0.05 relative to Ctrl. *P < 0.05 relative to DEP. **P < 0.001 relative to DEP.
Figure 9
Figure 9
Photomicrographs depicting the increased vascular adhesion molecule (VCAM) area in peribronchiolar vessels of lung tissue. In the DEP-treated group (b) compared to both the Ctrl group (a) and to the group that received 50 mg/kg of anacardic acids (c) (Immunohistochemistry). Scale bars = 25 μm.
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