Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
Eur Rev Med Pharmacol Sci. 2019 Apr;23(8):3542-3550. doi: 10.26355/eurrev_201904_17723.
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.
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.
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.
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.
褪黑素对阿尔茨海默病（AD）的作用和机制仍未得到充分研究。20E2 细胞（HEK293-APPswe 细胞）是 AD 的一种细胞模型。需要研究褪黑素对 20E2 细胞中线粒体结构和功能的调节作用。
评估阿尔茨海默病（AD）细胞模型的细胞活力、线粒体生物发生因子（过氧化物酶体增殖物激活受体γ共激活因子 1-α[PGC-1α]、核呼吸因子 1[NRF1]、核呼吸因子 2[NRF2]、线粒体转录因子 A[TFAM]）的表达水平、线粒体膜电位、Na+-K+-三磷酸腺苷酶（ATPase）和细胞色素 C 氧化酶活性、三磷酸腺苷（ATP）水平、线粒体 DNA/核 DNA（mtDNA/nDNA）比值以及有无褪黑素时的线粒体结构。
褪黑素提高了 20E2 细胞活力、线粒体生物发生因子（PGC-1α、NRF1、NRF2、TFAM）的表达、线粒体膜电位、Na+-K+-ATPase 和细胞色素 C 氧化酶活性、ATP 水平、mtDNA/nDNA 比值、线粒体结构，并减少了淀粉样前体蛋白的淀粉样生成处理。
通过 PGC-1α-NRF-TFAM 途径，线粒体生物发生障碍与 AD 的发病机制有关，褪黑素通过增强线粒体生物发生和减少阿尔茨海默病中淀粉样生成的 APP 处理来改善线粒体结构和功能。
