Abstract
This study aimed to investigate the direct effects of advanced glycation end products (AGEs) on the mitochondrial structure and function of SH-SY5Y cells and the possible molecular mechanism(s) underlying mitochondria dysfunction by AGEs. SH-SY5Y cells were cultured in 400 μg/ml of AGE-bovine serum albumin (BSA) for 24 h, and changes in the mitochondrial function of SH-SY5Y cells were analysed as follows. Reactive oxygen species (ROS) were detected using 2′,7′-dichlorodihydrofluorescein diacetate molecular probes. Mitochondrial membrane potential (ΔΨm) was determined by flow cytometry using fluorescent probes. The expression of cytochrome c (Cyt c) protein level was assessed by Western blotting. Mitochondrial structures were observed by transmission electron microscopy. Our results showed that AGE-BSA induced an increase in ROS levels, a decrease in mitochondrial ΔΨm, and the release of Cyt c from mitochondria in SH-SY5Y cells. The mitochondria of SH-SY5Y cells showed remarkable swelling and vacuolisation, but these changes were recovered after pretreatment with neutralising anti-receptor for advanced glycation end products (RAGE) antibody. Our results suggested that AGE-BSA induced mitochondrial dysfunction in SH-SY5Y cells through RAGE pathways. Thus, AGEs are potential mechanistic links between diabetes mellitus and Alzheimer’s disease.
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The study was supported by the Natural Science Foundation of China (81100810, 81203004) and the Postdoctoral Science Foundation of China (2013M540234).
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Editor: T. Okamoto
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Wang, X., Yu, S., Wang, CY. et al. Advanced glycation end products induce oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In Vitro Cell.Dev.Biol.-Animal 51, 204–209 (2015). https://doi.org/10.1007/s11626-014-9823-5
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DOI: https://doi.org/10.1007/s11626-014-9823-5