Neuroprotective effect of Hypericum perforatum extract against Aluminum-maltolate induced toxicity in SH-SY5Y cells

Abstract

Alzheimer's disease is multi-component neurodegenerative disorder. Oxidative stress disrupts regular functioning of metabolism in early-onset Alzheimer's disease. It causes Tau phosphorylation, formation of neurofibrillary tangle and neuron reduction. Due to intense binding of phosphorylated amino acids to aluminum, it induces self-assembly and deposition of high degree of phosphorylated cytoskeletal proteins, such as microtubule and neurofilament-associated proteins. In this study, it is aimed to consider the antioxidant potential of Hypericum perforatum extract against neurotoxicity caused by Aluminum-maltolate (Al(mal)3) and its effects on APP gene expression. Four different groups were determined to observe the impact of H. perforatum extract. After the incubation of the cells for 24 hours, only the medium was placed in the first group as control. 500 μM Al(mal)3 was added to the second group of cells. 20 μg mL-1 Hypericum perforatum extract was added to the third group. For the fourth group, 20 μg mL-1 Hypericum perforatum extract and 500 μM Al(mal)3 were added. While Al(mal)3 increased total antioxidant status levels in SH-SY5Y human neuroblastoma cells, H. perforatum extract significantly inhibited Al(mal)3 induced oxidative stress. On the other hand, H. perforatum extract significantly decreased APP gene expression levels depending on Al(mal)3 toxicity in SH-SY5Y cells. According to these results, H. perforatum extract significantly inhibited Al(mal)3 neurotoxicity against SH-SY5Y cells. To determine synergistic and antagonistic effects of H. perforatum extract content is important to examine their specific effects of together with hyperforin, which is a phytochemical produced by some of the members of the plant genus Hypericum, to discover new therapeutic agents against neurodegeneration.

Alzheimer ve Parkinson Hastalıklarında Bor İçeren Bileşiklerin Nörokoruyucu Etkisi

“…AH patolojisinin ayırt edici özelliği Amiloid β (Aβ) proteininin hücre dışı toplanmasıyla oluşan Aβ plakları ve hiperfosforile Tau proteini tarafından oluşan nörofibriler yumaklardır (NFT) [12]. AH'nin diğer ortak özellikleri; sinaptik hasar, sinaptik kayıp ve sinapslardaki yapısal değişiklikler gibi anormallikler ve işlev bozukluklarıdır [13].…”