Puerarin exhibits antiinflammatory properties in gunpowder smog-induced acute lung injury in rats via regulation of the renin-angiotensin system and the NFκB signaling pathway.

Abstract

Puerarin, which is a widely used in Traditional Chinese Medicine, was previously demonstrated to regulate the subsets of CD4+ lymphocytes in gunpowder smog-induced acute lung injury (ALI). However, the underlying mechanism remains largely unknown. Previous studies on autoimmune diseases have revealed that the renin-angiotensin system (RAS) and NF-κB participate in regulating the levels of CD4+ T lymphocytes. The aim of the present study was to further investigate the mechanisms underlying the protective effects of puerarin. Wistar rats were randomly divided into four groups as follows: Normal control, puerarin control, smoke inhalation injury and puerarin treatment plus smoke inhalation injury groups. The levels of angiotensin II (Ang II) in lung tissue and in the circulation, and the levels of interleukin (IL)-6, IL-1β, IL-17A and tumor necrosis factor (TNF)-α in the bronchoalveolar lavage fluid (BALF) were assayed using ELISA kits. The expression of Ang II type 1 receptor (AT1-R), angiotensin-converting enzyme (ACE) and ACE2 were examined by immunohistochemical analysis and western blotting. Phosphorylated (p-) NF-κB p65 and NF-κB inhibitor α (IκB-α) protein expression levels were also determined using western blotting. Puerarin treatment reduced the levels of inflammatory cytokines in the BALF. Furthermore, puerarin treatment significantly decreased the levels of Ang II, AT1-R and ACE, which were increased following smoke inhalation. Conversely, puerarin treatment upregulated the expression of ACE2, which was downregulated following smoke inhalation. Additionally, puerarin decreased the expression of p-NF-κB p65 and increased that of IkB-α. Thus, the antiinflammatory effects of puerarin were partly mediated via the RAS and via regulation of the NFĸB signaling pathway in rats with gunpowder smog-induced ALI.