Abstract
BackgroundAccumulative evidences have indicated that oxidative-stress and over-activation of N-methyl-d-aspartate receptors (NMDARs) are important mechanisms of brain injury. This study investigated the neuroprotection of Kukoamine A (KuA) and its potential mechanisms. MethodsMolecular docking was used to discover KuA that might have the ability of blocking NMDARs. Furthermore, the MTT assay, the measurement of LDH, SOD and MDA, the flow cytometry for ROS, MMP and Annexin V-PI double staining, the laser confocal microscopy for intracellular Ca2+ and western-blot analysis were employed to evaluate the neuroprotection of KuA. ResultsKuA attenuated H2O2-induced cell apoptosis, LDH release, ROS production, MDA level, MMP loss, and intracellular Ca2+ overload (both induced by H2O2 and NMDA), as well as increased the SOD activity. In addition, it could modulate the apoptosis-related proteins (Bax, Bcl-2, p53, procaspase-3 and procaspase-9), the SAPKs (ERK, p38), AKT, CREB, NR2A and NR2B expression. ConclusionsAll the results indicated that KuA has the ability of anti-oxidative stress and this effect may partly via blocking NMDARs in SH-SY5Y cells.General significance: KuA might have the potential therapeutic interventions for brain injury.
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Schedule a callMore From: Biochimica et Biophysica Acta (BBA) - General Subjects
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