Native Myeloperoxidase A & B (>96%)

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-alpha, IL-1 beta, 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-kappa B) activation was dose-dependently attenuated by fucoidan. Furthermore, fucoidan increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Glycogen synthase kinase3 beta (GSK-3 beta), and heme oxygenase (HO-1). In vitro, the results demonstrated that fucoidan or GSK-3 beta inhibitor significantly inhibited LPS-induced TNF-alpha production in A549 cells. And the inhibition of fucoidan on TNF-alpha 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 beta-Nrf2 signaling pathway.

The aim of this study was to investigate the effects of ampelopsin (AMP) on injuries of ovarian and lung tissues generated by bilateral ovarian torsion/detorsion (TD) model in rats. In the present study, 32 Sprague Dawley female rats were randomly divided into four groups. Groups planned as sham, TD, 80 mg/kg dose of AMP+TD, and 160 mg/kg dose of AMP+TD. In the sham group, the abdomen was opened applying an incision and closed again without TD model. In TD group, 3 hours of torsion followed 3 hours of detorsion were made. In the 80 and 160 mg/kg dose groups, respectively, AMP was given orally 80 and 160 mg/kg doses before detorsion and TD was performed as defined in TD group. At the end of detorsion period, rats were sacrificed and the ovarian and lung tissues were quickly removed. All results were analyzed using statistically appropriate tests. Malondialdehyde (MDA) level, myeloperoxidase (MPO) activity, tumor necrosis faktor-alpha (TNF-alpha), interleukin-lbeta (IL-1 beta), total oxidant status (TOS) and oxidative stress index (OSI) values increased significantly in TD group when compared to sham group (p <= 0.05). However, superoxide dismutase (SOD) enzyme activity and total antioxidant status (TAS) values decreased in ovarian and lung tissues of TD group. Conversely, SOD enzyme activity increased, while TOS and OSI values, MPO activity and TNF-alpha, IL-1 beta, MDA levels decreased significantly due to administration of AMP in 80 and 160 mg/kg dose groups (p <= 0.05). As a conclusion, in this study, it was demonstrated that 80 and 160 mg/kg doses of AMP administrations protected against oxidative damage of the ovarian and lung tissues that generated by experimental TD in rats.