Effect of phillygenin on inflammatory response of A549 cells induced by lipopolysaccharide and normal human plasma / 中国药理学通报

Aim To investigate the effect of phillygenin ( PHI) on lipopolysacchride ( LPS) and normal human plasma ( NHP) induced inflammatory injury on alveolar type II epithelial A549 cells and the related mechanism. Methods A549 cells were exposured to 1 mg • L

Astragalus polysaccharide regulates NF-κB/MAPK signaling pathway and attenuates airway inflammation in OVA-induced asthmatic rats / 中国药理学通报

Aim To detect the possible ameliorative effects of APS on the airway inflammation and whether the effects are associated with inhibiting the NF-κB/MAPK signaling pathway in ovalbumin( OVA)-induced asthmatic rats. Methods Asthma was induced by OVA sensitization and challenge. The asthmatic rats in the APS group were treated with APS. Pulmonary in-flammation was assessed with hematoxylin and eosin staining and inflammatory cell counting in BALF. Ul-trastructural changes of type I pneumocyte were ob-served by electron microscopy. Levels of NF-κB p65, p-NF-κB p65, p-IκBα, ERK1/2, p-ERK1/2, JNK, p-JNK, p38 MAPK, p-p38 MAPK, IL-1β, IL-4, IL-5 , IL-6 and IL-13 were measured using ELISA to as-sess the activity of NF-κB/ MAPK signaling pathway. Results Compared to the normal group, OVA in-duced significantly pulmonary inflammation and ultra-structural changes of type I pneumocyte in the asthma group. Besides, OVA increased the activity of the NF-κB/MAPK signaling pathway and promoted the produc-tion of inflammatory cytokines IL-1β, IL-4 , IL-5 , IL-6 and IL-13 in the asthma group. If compared to the asthma group, APS markedly attenuated the pulmonary inflammation and type I pneumocyte damage, as well as inhibited the activity of the NF-κB/MAPK signaling pathway and decreased the production of inflammatory cytokines in the APS group. Conclusion The amelio-rative effects of APS on airway inflammation might be associated with the inhibition of the activity of the NF-κB/MAPK signaling pathway.