Endothelin A receptor antagonist modulates lymphocyte and eosinophil infiltration, hyperreactivity and mucus in murine asthma

Landgraf, Richardt Gama; Jancar, Sônia

doi:10.1016/j.intimp.2008.08.014

Cited by 19 publications

(12 citation statements)

References 24 publications

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“…In fact, some papers have demonstrated that in BALB/c mice, the Th2 immune response develops a greater overall response when compared to C57BL/6 [23][24][25]. However, other authors have shown that C57BL/6 mice also exhibit marked pulmonary allergic inflammation compared to control animals [20,21,[26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Campanholle

Silva

Martins

et al. 2012

Cell Physiol Biochem

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The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). In addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. In addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors.

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Section: Discussionmentioning

confidence: 99%

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Campanholle

Silva

Martins

et al. 2012

Cell Physiol Biochem

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“…The respective ERA was each coadministered to dox or saline treated animals but one dox and one saline group each was kept without ERA treatment (controls). Dosage regime was adapted to published studies in rodents [14][15][16][17]. ERAs were applied every day starting 3 days before dox administration to reach effective plasma levels.…”

Section: Animals and Experimental Protocolsmentioning

confidence: 99%

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Schwebe

Ameling

Hammer

et al. 2015

Biochemical Pharmacology

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“…The concentration of 0.5% DMSO has been proved to be harmless in animals with i.p. injection [21,22]. Bosentan (Actelion Pharmaceuticals Japan Ltd, Tokyo, Japan) was prepared fresh each week as a suspension in 5% arabic gum and administered (100 mg?kg…”

Section: Experimental Protocolmentioning

confidence: 99%

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

Chen

Hanaoka²,

Droma³

et al. 2009

European Respiratory Journal

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We hypothesised that endothelin (ET)-1 plays an important role in the pathogenesis of emphysema. We attempted to apply ET-1 receptor antagonists to demonstrate and further elucidate the molecular pathogenesis pathways through which ET-1 may cause emphysematous changes.Sprague-Dawley rats were divided into four groups: control, cigarette smoke extract (CSE), CSE+BQ-123 (a selective endothelin receptor type A (ET A ) antagonist) and CSE+bosentan (a mixed ET A /ET B receptor antagonist). The CSE was injected intraperitoneally once a week for 3 weeks, and BQ-123 or bosentan was administered daily for the same duration. The expression of ET A receptor, apoptosis index, caspase-3 activity, matrix metalloproteinase (MMP)-2 and MMP-9 activity, and tumour necrosis factor (TNF)-a and interleukin (IL)-1b concentrations were measured in the lung tissue. The ET-1 levels and antioxidant activity were measured in the serum.Both BQ-123 and bosentan prevented the development of CSE-induced emphysema, blocked the expression of ET A receptor, inhibited pulmonary apoptosis, inactivated MMP-2 and MMP-9 activities in the lung tissues, reduced the concentrations of inflammatory cytokines TNF-a and IL1b, and improved the biological antioxidant activity in the serum.Emphysema development is suppressed by ET-1 receptor antagonists. ET-1 may cause emphysematous changes through molecular pathogenesis pathways involving apoptosis, proteinase and antiproteinase imbalance, inflammation and oxidative stress.

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Endothelin A receptor antagonist modulates lymphocyte and eosinophil infiltration, hyperreactivity and mucus in murine asthma

Cited by 19 publications

References 24 publications

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

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