Abstract
Veronicastrum axillare is a traditional medical plant in China which is widely used in folk medicine due to its versatile biological activities, especially for its anti-inflammatory effects. However, the detailed mechanism underlying this action is not clear. Here, we studied the protective effects of V. axillare against acute lung injury (ALI), and we further explored the pharmacological mechanisms of this action. We found that pretreatment with V. axillare suppressed the release of proinflammatory cytokines in the serum of ALI mice. Histological analysis of lung tissue demonstrated that V. axillare inhibited LPS-induced lung injury, improved lung morphology, and reduced the activation of nuclear factor-κB (NF-κB) in the lungs. Furthermore, the anti-inflammatory actions of V. axillare were investigated in vitro. We observed that V. axillare suppressed the mRNA expression of interleukin-1β (IL-1β), IL-6, monocyte chemotactic protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α) in RAW264.7 cells challenged with LPS. Furthermore, pretreatment of V. axillare in vitro reduced the phosphorylation of p65 and IκB-α which is activated by LPS. In conclusion, our data firstly demonstrated that the anti-inflammatory effects of V. axillare against ALI were achieved through downregulation of the NF-κB signaling pathway, thereby reducing the production of inflammatory mediators.
Highlights
Acute lung injury (ALI) is a prototypical inflammatory disease
These findings collectively suggest that V. axillare may be effective for ALI prevention induced by LPS
In order to research the mechanisms of V. axillare action, we used RAW264.7 cells to evaluate changes in inflammatory mediators, cytokines, and signaling pathways
Summary
Acute lung injury (ALI) is a prototypical inflammatory disease. ALI’s most significant pathological feature is the acute lung inflammation, including inflammatory cell recruitment and the release of proinflammatory mediators [1, 2]. LPS can be used to produce a classical animal model of ALI associated with the activation of monocytes, overflow of pulmonary neutrophils, increased levels of alveolar-capillary permeability, and diffuse alveolar damage [3]. During the initiation of the host defense process, LPS is recognized by Toll-like receptor 4 (TLR4), which activates several intracellular signaling pathways, among which nuclear factor-κB (NF-κB) pathway is the predominant one. The activation of NF-κB eventually leads to the upregulation of several inflammatory factors [4]. Interfering with NF-κB signaling pathway is a promising therapeutic regimen for the treatment of acute inflammatory disease, like ALI
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