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Abstract Title:

Fucoidan inhibits LPS-induced acute lung injury in mice through regulating GSK-3β-Nrf2 signaling pathway.

Abstract Source:

Arch Pharm Res. 2020 Jun ;43(6):646-654. Epub 2020 Jun 13. PMID: 32533502

Abstract Author(s):

De-Zhang Zhu, Yan-Ting Wang, Yan-Li Zhuo, Kong-Juan Zhu, Xiang-Zhen Wang, Ai-Jie Liu

Article Affiliation:

De-Zhang Zhu

Abstract:

The purpose of this study was to investigate the protective effects of fucoidan on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The mice were divided into the control, LPS, and LPS + fucoidan (20, 40, or 80 mg/kg) groups. LPS was given by intracheal instillation and fucoidan was given 1 h before LPS treatment. Myeloperoxidase (MPO) activity, malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione (GSH) contents, and inflammatory cytokine production were detected. The results showed that LPS-induced TNF-α, IL-1β, and IL-6 production, lung wet/dry (W/D) ratio, ROS, MDA content, and MPO activity were suppressed by fucoidan. The levels of SOD and GSH were increased by fucoidan. Meanwhile, LPS-induced nuclear factor kappa-B (NF-κB) activation was dose-dependently attenuated by fucoidan. Furthermore, fucoidan increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Glycogen synthase kinase3β (GSK-3β), and heme oxygenase (HO-1). In vitro, the results demonstrated that fucoidan or GSK-3β inhibitor significantly inhibited LPS-induced TNF-α production in A549 cells. And the inhibition of fucoidan on TNF-α production was blocked by Nrf2 siRNA. This study showed fucoidan protected mice against LPS-induced ALI through inhibiting inflammatory and oxidative responses via regulating GSK-3β-Nrf2 signaling pathway.

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