Abstract
Gastrodin (GAS), a phenolic glucoside derived from Gastrodiaelata Blume, has been reported to have anti-inflammatory effect. The aim of this study was to investigate the effects of GAS on LPS-induced acute lung injury in mice. ALI was induced by the intranasal administration of LPS and GAS was given 1 h or 12 h after LPS treatment. The results indicated that GAS treatment markedly attenuated the damage of lung injury induced by LPS. GAS attenuated the activity of myeloperoxidase (MPO) and down-regulated the levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in BALF. LPS-induced lung edema and lung function were also reversed by GAS. Furthermore, GAS was found to inhibit LPS-induced inflammatory cells infiltration. In addition, treatment of GAS inhibited LPS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. In conclusion, our results indicated that GAS had anti-inflammatory effects on LPS-induced acute lung injury. The anti-inflammatory mechanism of GAS was through the inhibition of NF-κB and activation of Nrf2 signaling pathways.
Highlights
Acute lung injury (ALI), the inflammation of the lung tissue, is a highly prevalent disease [1]
A large body of evidences showed that inhibition of inflammation may have protective effects against ALI [27]
We demonstrated that gastrodin protected against LPSinduced ALI by inhibiting inflammatory response
Summary
Acute lung injury (ALI), the inflammation of the lung tissue, is a highly prevalent disease [1]. It is characterized by hypoxemia and pulmonary edema in lung [2]. Recent studies showed that inflammatory response played a critical role in the pathogenesis of ALI [3, 4]. LPS induces the release of inflammatory cytokine including TNF-α and IL-1β, which exacerbate harmful immune responses [5, 6]. Previous studies suggested that inhibition the release of inflammatory cytokines could treat ALI [5, 7]. Inhibition of NF-κB activation could attenuate LPS-induced ALI [9]
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