Tubastrine, an antioxidant molecule from Tubastraea tagusensis sun coral, in the reversion of oxidative stress and neuron's death induced by Aβ42.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder involving mitochondrial dysfunction and consequent production of reactive oxygen species (ROS), generated after amyloid peptide (Aβ42) accumulation. In this study, we isolated a new antioxidant molecule from the sun coral Tubastraea tagusensis and analysed it in cells exposed to oligomeric amyloid-beta peptide 1-42 (oAβ42). The coral was collected and immersed in methanol for the release of compounds, which were submitted to antioxidant DPPH and FRAP activity-guided fractionation using solid-phase extraction and HPLC. An active pure molecule was analysed by mass spectrometry and tested in SH-SY5Y differentiated neurons previously exposed to 5 μM oAβ42. The isolated active molecule was identified as tubastrine, which could significantly inhibit the cell death caused by the amyloid peptide. Moreover, oAβ42 increased the percentage of ROS in neurons-like from 40% to 65%, and the treatment with tubastrine reduced it to 50%. The antioxidant power of neurons-like after oAβ42 decreased significantly, while the compound reversed it, reaching similar values to the untreated cells. Therefore, tubastrine can reverse an important pathophysiological mechanism of AD, oxidative stress, by increasing neuronal antioxidant power and reducing ROS levels, able to prevent neuron-like cell death caused by oAβ42.