Therapeutic effects of rosmarinic acid on airway responses in a murine model of asthma |
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| Affiliation: | 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;1. Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea;2. High-Enthalpy Plasma Research Center, Chonbuk National University, Republic of Korea;3. Division of Marine Environment & Bioscience, Korea Maritime University, Busan, Republic of Korea;4. Biochip Research Center and Inflammatory Disease Research Center, Hoseo University, 165, Sechul-ri, Baebang-myun, Asan, Chungnam 336-795, Republic of Korea;5. Regional Innovation Center and Inflammatory Disease Research Center, Hoseo University, 165, Sechul-ri, Baebang-myun, Asan, Chungnam 336-795, Republic of Korea;6. Oriental Bio-herb Research Institute, Kangwon National University, Chuncheon 200-701, Republic of Korea;7. School of Biomedical Sciences, Charles Sturt University, Bathurst, NSW 2795, Australia;1. Xinjiang Institute of Materia Medica, Urumqi 830004, China;2. Xinjiang Uygur Autonomous Region for Food and Drug Control, Urumqi 830002, China;3. Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050,China |
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| 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 (20 mg/kg) 1 h 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. |
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