Apelin-13 protects human neuroblastoma SH-SY5Y cells against amyloid-beta induced neurotoxicity: Involvement of anti oxidant and anti apoptotic properties

Mohammad Rasoul Samandari-Bahraseman; Leila Elyasi

doi:10.1515/jbcpp-2020-0294

Article

Apelin-13 protects human neuroblastoma SH-SY5Y cells against amyloid-beta induced neurotoxicity: Involvement of anti oxidant and anti apoptotic properties

Mohammad Rasoul Samandari-Bahraseman and Leila Elyasi

Published/Copyright: May 10, 2021

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From the journal Journal of Basic and Clinical Physiology and Pharmacology Volume 33 Issue 5

Abstract

Objectives

We investigated the effect of apelin-13 on the cellular model of AD, amyloid-β (Aβ) treated SH-SY5Y cells in rats.

Methods

The SH-SY5Y cells were pretreated with different doses of apelin-13 (1, 2.5, 5, and 10 μg/mL), half an hour before adding 50% Aβ treatment. After 24 h, cells were evaluated for survival, oxidative stress, mitochondrial calcium release, caspase-3, and cytochrome c levels, compared to control group (beta-actin). Statistical analysis was performed by SPSS 16.

Results

Apelin-13 at the dose of 2.5 μg/mL protected against IC50 Aβ (p<0.001). Apelin-13 at doses of 1, 2.5, and 5 μg/mL showed protective effects against the reactive oxygen species (ROS) produced by Aβ (p<0.001). Apelin-13 at doses of 2.5 and 5 μg/mL reduced calcium release, caspase-3, and cytochrome c (all p<0.001).

Conclusions

Apelin-13 prevented apoptosis, oxidative stress, and mitochondrial toxicity and can be a suitable option for treatment of AD. The appropriate treatment strategy for humans has to be investigated in future studies.

Keywords: Apelin; Alzheimer disease; neuroprotective agents; oxidative stress

Key Messages: Apelin-13 prevented apoptosis, oxidative stress, and mitochondrial toxicity in SH-SY5Y cells that were pretreated with different doses of Apelin (1, 2.5, 5, and 10 μg/mL), half an hour before adding 50% amyloid-β (Aβ) treatment; thus, it can be a suitable option for treatment of AD

Corresponding author: Leila Elyasi, Golestan Neuroscience Research Center (GNRC), Department of Anatomy, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran, Phone: +98 9113932235, E-mail: elyasi@goums.ac.ir

Acknowledgements

None

Research funding: None declared.
Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission.
Competing interests: Authors state no conflict of interest.
Informed consent: Informed consent was not necessary in this study.
Ethical approval: The study was approved by the Ethics Committee of Gorgan University of Medical Sciences (IR.GOUMS.REC.1397.171).

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Received: 2020-09-06

Accepted: 2021-04-20

Published Online: 2021-05-10

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Articles in the same Issue

https://doi.org/10.1515/jbcpp-2020-0294

Keywords for this article

Apelin; Alzheimer disease; neuroprotective agents; oxidative stress; Apelin-13 prevented apoptosis, oxidative stress, and mitochondrial toxicity in SH-SY5Y cells that were pretreated with different doses of Apelin (1, 2.5, 5, and 10 μg/mL), half an hour before adding 50% amyloid-β (Aβ) treatment; thus, it can be a suitable option for treatment of AD