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Int Immunopharmacol. 2016 Dec;41:90-97. doi: 10.1016/j.intimp.2016.10.010. Epub 2016 Nov 5.

Therapeutic effects of rosmarinic acid on airway responses in a murine model of asthma.

Author information

1
College of Animal Science and Technology, Guangxi University, Nanning, Guangxi 530005, PR China.
2
Guangxi Engineering Research Center for Veterinary Medicine, Nanning, Guangxi 530007, PR China.
3
College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin 130062, PR China.
4
College of Animal Science and Technology, Guangxi University, Nanning, Guangxi 530005, PR China. Electronic address: ahong18@vip.sina.com.

Abstract

Rosmarinic acid (RA) is an active component of a traditional Chinese herbal medicine. Previously, we reported that RA exerted a strong anti-inflammatory effect in a mouse acute lung injury model. Therefore, we hypothesized that RA might also have potential therapeutic effects in a murine model of asthma. In this study, we aimed to evaluate the anti-asthmatic activity of RA and explored its possible molecular mechanisms of action. Female BALB/c mice that had been sensitized to and challenged with ovalbumin (Ova) were treated with RA (20mg/kg) 1h after challenge. The results showed that RA greatly diminished the number of inflammatory cells and the production of Th2 cytokines in the bronchoalveolar lavage fluid (BALF); significantly reduced the secretion of total IgE, Ova-specific IgE, and eotaxin; and markedly ameliorated airway hyperresponsiveness (AHR) compared with Ova-induced mice. Histological studies further revealed that RA substantially decreased inflammatory cells infiltration and mucus hypersecretion compared with Ova-induced mice. Moreover, our results suggested that the protective effects of RA were mediated by the inhibition of JNK and p38 MAPK phosphorylation and nuclear factor-κB (NF-κB) activation. Furthermore, RA treatment resulted in a significant reduction in the mRNA expression of AMCase, CCL11, CCR3, Ym2 and E-selectin in lung tissue. These findings suggest that RA may effectively delay the development of airway inflammation and could thus be used as a therapy for allergic asthma.

KEYWORDS:

AHR; Allergic airway inflammation; MAPK; NF-κB; Rosmarinic acid; Therapeutic

PMID:
27825045
DOI:
10.1016/j.intimp.2016.10.010
[Indexed for MEDLINE]

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