AI Article Synopsis
- Catalpol, an iridiod glucoside from Rehmannia glutinosa, shows promising anti-inflammatory effects, particularly in lung protection, which had not been previously studied.
- The study examined its impact on lung injury induced by lipopolysaccharide (LPS) in a mouse model, revealing that catalpol significantly reduced lung injury markers and inflammatory cytokines.
- The research concluded that catalpol's protective effects are linked to its ability to inhibit specific signaling pathways (TLR4-mediated NF-κB and MAPK) associated with inflammation.
Article Abstract
Catalpol, an iridiod glucoside isolated from Rehmannia glutinosa, has been reported to have anti-inflammatory properties. Although anti-inflammatory activity of catalpol already reported, its involvement in lung protection has not been reported. Thus, we investigated the role of catalpol on lipopolysaccharide (LPS)-induced acute lung injury in this study. Mice acute lung injury model was induced by intranasal instillation of LPS. Catalpol was administrated 1h prior to or after LPS exposure. The severity of pulmonary injury was evaluated 12h after LPS administration. The results showed that catalpol inhibited lung W/D ratio, myeloperoxidase activity of lung samples, the amounts of inflammatory cells and TNF-α, IL-6, IL-4 and IL-1β in BALF induced by LPS. The production of IL-10 in BALF was up-regulated by catalpol. In vitro, catalpol inhibited TNF-α, IL-6, IL-4 and IL-1β production and up-regulated IL-10 expression in LPS-stimulated alveolar macrophages. Moreover, western blot analysis showed that the activation of NF-κB and MAPK signaling pathways was inhibited by catalpol. Furthermore, catalpol was found to inhibit TLR4 expression induced by LPS. In conclusion, catalpol potently protected against LPS-induced ALI. The protective effect may attribute to the inhibition of TLR4-mediated NF-κB and MAPK signaling pathways.
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| http://dx.doi.org/10.1016/j.intimp.2014.07.011 | DOI Listing |
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