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Published:
May 12, 2021DOI:
10.4314/tjpr.v18i3.2Keywords:
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Main Article Content
Withdrawn: Safranal induces autophagy by AMPK activation and protects neurons against amyloid beta in Alzheimer’s disease
Abstract
This article has been withdrawn by the Editor
Purpose: To investigate autophagic induction by safranal and neuroprotection against amyloid beta in Alzheimer’s disease.
Methods: Primary neurons and SH-SY5Y cells were used in this study. Assessment of cell proliferation and neuroprotection by safranal against amyloid beta was done by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. AMPK activation and mTOR inhibition were determined by western blot. Changes in intracellular calcium level, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were assessed by flow cytometry.
Results: Safranal protected neurons against amyloid beta toxicity. Furthermore, safranal activated AMPK pathway by activation of calcium/calmodulin-dependent protein kinase (CaMKKβ) to induce autophagy in both cell lines. The toxicity induced by amyloid beta in primary neurons and SH-SY5Y cells were attenuated by safranal. Moreover, amyloid beta-induced calcium levels were significantly decreased by safranal while ROS and MMP loss produced by amyloid beta was attenuated by safranal.
Conclusion: These findings suggest that safranal protects neurons against amyloid beta by inducing autophagy via AMPK pathway. Therefore, safranal is a probable therapeutic target for Alzheimer’s disease.
