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Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling

Authors :
Chaemoon Lim
Ao Xuan Zhen
Sungwoo Ok
Pincha Devage Sameera Madushan Fernando
Herath Mudiyanselage Udari Lakmini Herath
Mei Jing Piao
Kyoung Ah Kang
Jin Won Hyun
Source :
Antioxidants, Vol 11, Iss 9, p 1707 (2022)
Publication Year :
2022
Publisher :
MDPI AG, 2022.

Abstract

Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, has been reported to scavenge free radicals. Only a few studies have explored the protective effects of hesperidin against high glucose−induced apoptosis in SH−SY5Y neuronal cells. Glucose stimulated neuronal cells to generate excessive ROS and caused DNA damage. In addition, glucose triggered endoplasmic reticulum stress and upregulated cytoplasmic as well as mitochondrial calcium levels. Hesperidin inhibited glucose−induced ROS production and mitigated the associated DNA damage and endoplasmic reticulum stress. The downregulation of antiapoptotic protein Bcl−2 following glucose treatment was reversed by a hesperidin treatment. Furthermore, hesperidin repressed the glucose−induced Bcl−2−associated X protein, cleaved caspase−9, and cleaved caspase−3. Hesperidin also suppressed the glucose−induced phosphorylation of extracellular signal−regulated kinase and c−Jun N−terminal kinase. The current results confirmed that hesperidin could protect neuronal cells against glucose−induced ROS. Mechanistically, hesperidin was shown to promote cell viability via attenuation of the mitogen−activated protein kinase signaling pathway.

Details

Language :
English
ISSN :
20763921
Volume :
11
Issue :
9
Database :
Directory of Open Access Journals
Journal :
Antioxidants
Publication Type :
Academic Journal
Accession number :
edsdoj.6b4ed04f3c74a3e81307dac71f47daa
Document Type :
article
Full Text :
https://doi.org/10.3390/antiox11091707