Abstract
Asthma is characterized by airway inflammation and mucus hypersecretion. Curcumin possessed a potent anti-inflammatory property involved in the PPARγ-dependent NF-κB signaling pathway. Then, the aim of the current study was to explore the value of curcumin in asthmatic airway inflammation and mucus secretion and its underlying mechanism. In vivo, mice were sensitized and challenged by ovalbumin (OVA) to induce chronic asthma. Airway inflammation and mucus secretion were analyzed. In vitro, BEAS-2B cells were obtained. MCP-1, MUC5AC, and PPARγ expression and the phosphorylation of NF-κB p65 and NF-κB p65 DNA-binding activity were measured in both the lungs and BEAS-2B cells. shRNA-PPARγ was used to knock down PPARγ expression. We found that OVA-induced airway inflammation and mucus hypersecretion in mice, OVA and IL-4-induced upregulation of MCP-1 and MUC5AC, suppression of PPARγ, and activation and translocation of NF-κB p65 were notably improved by curcumin both in vivo and in vitro. Our data also showed that these effects of curcumin were significantly abrogated by shRNA-PPARγ. Taken together, our results indicate that curcumin attenuated OVA-induced airway inflammation and mucus hypersecretion in mice and suppressed OVA- and IL-4-induced upregulation of MCP-1 and MUC5AC both in vivo and in vitro, most likely through a PPARγ-dependent NF-κB signaling pathway.
Highlights
Airway inflammation and mucus hypersecretion are two of the most important characteristics of chronic asthma [1,2,3]
Many studies confirmed that a broad spectrum of inflammatory mediators, such as IL-4, IL-5, and IL-13, synthesized and released by activated inflammatory cells, Th2 cells, eventually induce airway mucus hypersecretion which is essential for the pathogenesis of asthma [3, 5]
This effect of curcumin was significantly blunted by shRNA-PPARγ
Summary
Airway inflammation and mucus hypersecretion are two of the most important characteristics of chronic asthma [1,2,3]. Many studies confirmed that a broad spectrum of inflammatory mediators, such as IL-4, IL-5, and IL-13, synthesized and released by activated inflammatory cells, Th2 cells, eventually induce airway mucus hypersecretion which is essential for the pathogenesis of asthma [3, 5]. Green et al showed that bronchial mucous glands, resulting in mucous plugs within the airway lumen and ectasia of the gland ducts, are increased in fatal asthma and may contribute to asphyxia due to mucous plugging in the autopsy, compared with nonfatal asthma and nonasthma [7]. At present, there is still no effective treatment for airway mucus hypersecretion. New therapeutic treatments for this unmet medical need are meaningful and valuable
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