Department of Respiration, Huaihe Hospital of Henan University, Ximen Street No. 115, Kaifeng, 475000, People's Republic of China.
Inflammation. 2018 Jun;41(3):795-802. doi: 10.1007/s10753-018-0733-7.
It has been reported that plantamajoside (PMS), a major natural compound isolated from Plantago asiatica, has anti-inflammatory activities. However, the effect of PMS on respiratory inflammatory diseases has not yet been studied. The present study aimed to evaluate the effect of PMS on lipopolysaccharide (LPS)-induced airway inflammation and the underlying mechanism. The results showed that PMS did not affect the cell viability of 16-HBE cells. PMS (20 and 40 μg/ml) decreased the expression levels of MUC5AC, IL-6, and IL-1β, which were induced by LPS treatment. PMS inhibited the LPS-induced phosphorylation of Akt and p65. In addition, inhibitors of the PI3K/Akt and NF-κB pathways attenuated the effect of LPS on 16-HBE cells. In conclusion, PMS inhibits LPS-induced MUC5AC expression and inflammation through suppressing the PI3K/Akt and NF-κB signaling pathways, indicating that PMS may be a potential therapy for the treatment of respiratory inflammatory diseases.
据报道,车前草苷(PMS)是从车前草中分离得到的一种主要天然化合物,具有抗炎活性。然而,PMS 对呼吸道炎症性疾病的影响尚未得到研究。本研究旨在评估 PMS 对脂多糖(LPS)诱导的气道炎症的作用及其机制。结果表明,PMS 不影响 16-HBE 细胞的细胞活力。PMS(20 和 40μg/ml)降低了 LPS 处理诱导的 MUC5AC、IL-6 和 IL-1β 的表达水平。PMS 抑制了 LPS 诱导的 Akt 和 p65 的磷酸化。此外,PI3K/Akt 和 NF-κB 通路的抑制剂减弱了 LPS 对 16-HBE 细胞的作用。综上所述,PMS 通过抑制 PI3K/Akt 和 NF-κB 信号通路抑制 LPS 诱导的 MUC5AC 表达和炎症,表明 PMS 可能是治疗呼吸道炎症性疾病的一种潜在疗法。