Respiratory Medicine, Second Affiliated Hospital of Chongqing Medical University, 400010 Chongqing, China.
Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai 20032, China.
Mediators Inflamm. 2019 Apr 3;2019:4927430. doi: 10.1155/2019/4927430. eCollection 2019.
Asthma is characterized by airway inflammation and mucus hypersecretion. Curcumin possessed a potent anti-inflammatory property involved in the PPAR-dependent NF-B 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 PPAR expression and the phosphorylation of NF-B p65 and NF-B p65 DNA-binding activity were measured in both the lungs and BEAS-2B cells. shRNA-PPAR was used to knock down PPAR 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 PPAR, and activation and translocation of NF-B 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-PPAR. 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 PPAR-dependent NF-B signaling pathway.
哮喘的特征是气道炎症和黏液过度分泌。姜黄素具有强大的抗炎特性,涉及 PPAR 依赖性 NF-B 信号通路。本研究旨在探讨姜黄素在哮喘气道炎症和黏液分泌中的价值及其潜在机制。体内,卵清蛋白(OVA)致敏和激发诱导慢性哮喘,分析气道炎症和黏液分泌。体外,获得 BEAS-2B 细胞。检测肺和 BEAS-2B 细胞中 MCP-1、MUC5AC 和 PPAR 的表达以及 NF-B p65 的磷酸化和 NF-B p65 DNA 结合活性。用 shRNA-PPAR 敲低 PPAR 表达。结果发现,姜黄素显著改善了 OVA 诱导的小鼠气道炎症和黏液过度分泌、OVA 和 IL-4 诱导的 MCP-1 和 MUC5AC 上调、PPAR 抑制以及 NF-B p65 的激活和转位。我们的数据还表明,shRNA-PPAR 显著削弱了姜黄素的这些作用。综上所述,我们的结果表明,姜黄素减轻了 OVA 诱导的小鼠气道炎症和黏液过度分泌,并抑制了 OVA 和 IL-4 诱导的 MCP-1 和 MUC5AC 上调,可能通过 PPAR 依赖性 NF-B 信号通路。