Ent of Nutrition Science, Purdue University, West Lafayette, IN 47907, USA Master Program in Meals Safety, Taipei Health-related University, Taipei 110, Taiwan Correspondence: [email protected]; Tel.: +886-2-2736-1661 (ext. 6555); Fax: +886-2-2737-3112 These authors contributed equally to this work.Citation: Ho, C.-L.; Kao, N.-J.; Lin, C.-I.; Cross, T.-W.L.; Lin, S.-H. Quercetin Increases Mitochondrial Biogenesis and Reduces Absolutely free Radicals in Neuronal SH-SY5Y Cells. Nutrients 2022, 14, 3310. doi.org/ ten.3390/nu14163310 Academic Editors: Luisa Cigliano, Maria Stefania Spagnuolo and Arianna Mazzoli Received: 8 July 2022 Accepted: 9 August 2022 Published: 12 August 2022 Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Abstract: Alzheimer’s illness (AD) is really a frequent neurodegenerative disorder that causes dementia and affects millions of folks worldwide. The mechanism underlying AD is unclear; even so, oxidative pressure and mitochondrial biogenesis happen to be reported to be involved in AD progression. Preceding investigation has also reported the reduction in mitochondrial biogenesis inside the brains of sufferers with AD. Quercetin (QE), a sort of polyphenol, has been identified to become capable of escalating mitochondrial biogenesis in the body. Accordingly, we explored irrespective of whether QE could lessen amyloid beta (A) accumulation triggered by hydrogen peroxide (H2 O2 )-induced oxidative anxiety in SH-SY5Y cells. Our benefits revealed that QE stimulated the expression of mitochondrial-related proteins such as SIRT1, PGC-1, and TFAM and subsequently activated mitochondrial biogenesis. Furthermore, QE improved ADAM10 expression but lowered H2 O2 -induced reactive oxygen species production, apoptosis, -site amyloid precursor protein cleaving enzyme 1 expression, and also a accumulation inside the SH-SY5Y cells. These findings indicate that QE can properly elevate mitochondrial biogenesisrelated proteins and minimize the damage caused by oxidative strain, making it a promising choice for protecting neuronal cells.IL-6 Protein Source Keyword phrases: A; oxidative pressure; quercetin; mitochondrial biogenesis; neurodegenerative disease1.MMP-1 Protein medchemexpress Introduction Aging is characterized by the progressive loss of tissue and organ function, which can be connected for the accumulation of reactive oxygen species (ROS)-mediated oxidative damage [1,2].PMID:23891445 Oxidative stress not simply impacts aging but can also be involved in several age-related situations including cardiovascular illness, chronic obstructive pulmonary disease, chronic kidney disease, cancer, and neurodegenerative illnesses. Alzheimer’s disease (AD) is often a widespread neurodegenerative disease that causes dementia and impacts millions of persons worldwide; presently, only symptomatic remedies are offered for AD [3]. Despite the fact that the mechanism underlying AD is unclear, oxidative tension and mitochondrial biogenesis have been reported to be involved within the progression of AD [1,4]. Oxidative anxiety is characterized by the overproduction of ROS, which can induce mitochondrial DNA (mtDNA) mutations, harm the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2+ homeostasis and mitochondrial defense systems. Hydrogen peroxide (H2 O2 ), a product of superoxide dismutase (SOD) dismutation, is among the ROS that engender oxidative strain [5]. H2 O2 accumulation may well bring about protein oxidization, cell membrane lipid oxidation, and DNA strand breakage [6], which may perhaps cause cell apoptosis [7]. Mitochondria play a k.
