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Updated: Aug 2, 2026

Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
Published on: July 30, 2016
Protective effects of melatonin on mitochondrial biogenesis and mitochondrial structure and function in the
1Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China. xie_zhaohong@126.com.
Objective:
The effects and mechanisms of melatonin on Alzheimer's disease (AD) are still not researched thoroughly. 20E2 cells (HEK293-APPswe cells) are a cellular model of AD. The modulation effects of melatonin on the structure and function of mitochondria in 20E2 cells need to be studied.
Materials And Methods:
The Alzheimer's disease (AD) cell model was assessed for cell viability, expression levels of mitochondrial biogenesis factors (peroxisome proliferator-activated receptor gamma coactivator 1-alpha [PGC-1α], nuclear respiratory factor 1 [NRF1], nuclear respiratory factor 2 [NRF2], mitochondrial transcription factor A [TFAM]), mitochondrial membrane potential, Na+-K+-adenosine triphosphatase (ATPase) and cytochrome C oxidase activity, adenosine triphosphate (ATP) level, mitochondrial DNA/nuclear DNA (mtDNA/nDNA) ratio, and mitochondrial structure with and without melatonin.
Results:
Melatonin improved 20E2 cell viability, expression of mitochondrial biogenesis factors (PGC-1α, NRF1, NRF2, TFAM), mitochondrial membrane potential, Na+-K+-ATPase, and cytochrome C oxidase activity, ATP level, mtDNA/nDNA ratio, mitochondrial structure, and decreased amyloidogenic amyloid precursor protein processing.
Conclusions:
Mitochondrial biogenesis disorder is associated with the pathogenesis of AD through PGC-1α-NRF-TFAM pathway, and melatonin improves the mitochondrial structure and function by enhancing mitochondrial biogenesis and decreasing amyloidogenic APP processing in Alzheimer's disease.
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