Abstract
Quercetin is a bioflavonoid with potential antioxidant properties. However, the mechanisms underlying its effects remain unclear. Herein, we focused on integrating long noncoding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) sequencing of PC-12 cells treated with quercetin. We treated PC-12 cells with hydrogen peroxide to generate a validated oxidative damage model. We evaluated the effects of quercetin on PC-12 cells and established the lncRNA, miRNA, and mRNA profiles of these cells. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of these RNAs were conducted to identify the key pathways. Quercetin significantly protected PC-12 neuronal cells from hydrogen peroxide-induced death. We identified 297, 194, and 14 significantly dysregulated lncRNAs, miRNAs, and mRNAs, respectively, associated with the antioxidant effect of quercetin. Furthermore, the phosphatidylinositol-3-kinase/protein kinase B pathway was identified as the crucial signalling pathway. Finally, we constructed a lncRNA-associated competing endogenous RNA (ceRNA) network by utilizing oxidative damage mechanism-matched miRNA, lncRNA, and mRNA expression profiles and those changed by quercetin. In conclusion, quercetin exerted a protective effect against oxidative stress-induced damage in PC-12 cells. Our study provides novel insight into ceRNA-mediated gene regulation in the progression of oxidative damage and the action mechanisms of quercetin.
Highlights
The maintenance of normal physiological functions depends on the balance between reactive oxygen species (ROS) and intracellular antioxidant factors
The protective effect of QUE on PC-12 cell viability rate induced by H2O2 was detected by the MTS assay
Through treatment with QUE, the survival rate of PC-12 cells was significantly increased in a dose-dependent manner (p < 0:05)
Summary
The maintenance of normal physiological functions depends on the balance between reactive oxygen species (ROS) and intracellular antioxidant factors. Numerous age-related and neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and inherited mitochondrial disorders, are directly associated with OS [6,7,8] Considering this relationship, extensive research is focused on uncovering the underlying mechanisms and role of OS in the onset and development of disease. By competing to bind to miRNA-150, lncRNA FOXD3AS1 blocked its protective effect, thereby contributing to the OS-induced apoptosis of lung epithelial cells [23]. Overall, these studies indicated that the link between ncRNAs and OS is stronger than previously thought. Transcriptomics and bioinformatics analyses were conducted to further investigate the regulatory mechanisms of QUE in protecting neuronal cells from oxidative damage
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