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KMID : 0043320200430060646
Archives of Pharmacal Research
2020 Volume.43 No. 6 p.646 ~ p.654
Fucoidan inhibits LPS-induced acute lung injury in mice through regulating GSK-3¥â-Nrf2 signaling pathway
Zhu De-Zhang

Wang Yan-Ting
Zhuo Yan-Li
Zhu Kong-Juan
Wang Xiang-Zhen
Liu Ai-Jie
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-¥á, IL-1¥â, 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-¥êB) activation was dose-dependently attenuated by fucoidan. Furthermore, fucoidan increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Glycogen synthase kinase3¥â (GSK-3¥â), and heme oxygenase (HO-1). In vitro, the results demonstrated that fucoidan or GSK-3¥â inhibitor significantly inhibited LPS-induced TNF-¥á production in A549 cells. And the inhibition of fucoidan on TNF-¥á 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-3¥â-Nrf2 signaling pathway.
KEYWORD
LPS, Fucoidan, Lung injury, Nrf2
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