Xiaocheng Huang,
Manlian Zhu,
Ying Hua,
Xiumei Yan,
Ruilai Jiang 
For correspondence:- Ruilai Jiang Email: JosegCarterqa@yahoo.com Tel:+865782559898
Accepted: 21 February 2019 Published: 31 March 2019
Citation: Huang X, Zhu M, Hua Y, Yan X, Jiang R. Safranal induces autophagy by AMPK activation and protects neurons against amyloid beta in Alzheimer disease. Trop J Pharm Res 2019; 18(3):459-464 doi: 10.4314/tjpr.v18i3.2
© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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.
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