Abstract
Rosmarinic acid (RA) has numerous pharmacologic effects, including anti-oxidant, anti-inflammatory, and analgesic effects. This study aimed to evaluate the preventive activity of RA in a murine model of asthma and to investigate its possible molecular mechanisms. Female BALB/c mice sensitized and challenged with ovalbumin (Ova) were pretreated with RA (5, 10 or 20 mg/kg) at 1 h before Ova challenge. The results demonstrated that RA markedly inhibited increases in inflammatory cells and Th2 cytokines in the bronchoalveolar lavage fluid (BALF), significantly reduced the total IgE and Ova-specific IgE concentrations, and greatly ameliorated airway hyperresponsiveness (AHR) compared with the control Ova-induced mice. Histological analyses showed that RA substantially decreased the number of inflammatory cells and mucus hypersecretion in the airway. In addition, our results suggested that the protective effects of RA might be mediated by the suppression of ERK, JNK and p38 phosphorylation and activation of nuclear factor-κB (NF-κB). Furthermore, RA pretreatment resulted in a noticeable reduction in AMCase, CCL11, CCR3, Ym2 and E-selectin mRNA expression in lung tissues. These findings suggest that RA may effectively delay the progression of airway inflammation.
Highlights
IntroductionThe incidence, morbidity and mortality of this disease have been increasing at remarkable rates over the last few decades, especially in industrialized countries [2,3]
Asthma is a serious health problem that affects people of all ages [1]
We have found that Rosmarinic acid (RA)
Summary
The incidence, morbidity and mortality of this disease have been increasing at remarkable rates over the last few decades, especially in industrialized countries [2,3]. It is closely related to increased production of various inflammatory mediators, cytokines and adhesion molecules [5,6]. The Th2 cytokines IL-4, IL-5 and IL-13, which are secreted from Th2 cells, have been demonstrated to play important roles in allergic airway inflammation [6,7,8]. Airway eosinophilia and Th2 cytokines may contribute to AHR in asthma [4]. It is well known that eosinophils that respond to a variety of CC chemokines, such as CCL11 (eotaxin), CCL24 (eotaxin-2) and CCL26 (eotaxin-3), are proinflammatory granulocytes with significant roles in several inflammatory diseases, including asthma [10,11]
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