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Neurons exposed to Aβ will be apoptotic in Alzheimer's disease (AD) brains or in vitro. The aim of the current study is to explore the neuroprotective mechanism that 7,8-dithydroxycoumarin inhibits JNK and p38MAPK-mediated Aβ-induced neurotoxicity. In vitro cultures of SH-SY5Y human neuroblastoma cell lines were treated with 7,8-dithydroxycoumarin (0, 1, 5 and 10 μmol/L) for 1.5 h, subsequently treated with 25 μmol/L Aβ25-35 fibrils. The MTT method was used to detect cell proliferation, and fluorescence probe H2DCF-DA was used to determine intracellular reactive oxygen species (ROS) content. Western-blot assay was performed to detect the JNK and P38MAPK phosphorylation. 25 μmol/L Aβ25-35 fibrils suppressed cell growth. They increased intracellular ROS, and enhanced levels of JNK and P38MAPK phosphorylation in a time-dependent manner. 7,8-dithydroxycoumarin treatment improved cell proliferation, reduced ROS generation and down-regulated levels of JNK and p38MAPK phosphorylation in a concentration-dependent manner. 7,8-dithydroxycoumarin may inhibit Aβ-induced neurotoxic injury through suppressing ROS, JNK and p38MAPK pathways. The finding of the current study is conducive to protecting neurons in AD by using 7,8-dithydroxycoumarin.
& beta,-amyloid, Oxidative Stress, 7,8-dithydroxycoumarin, neuroprotection, JNK, p38MAPK, #