Protection against HEMA-Induced Mitochondrial Injury In Vitro by Nrf2 Activation
| العنوان: | Protection against HEMA-Induced Mitochondrial Injury In Vitro by Nrf2 Activation |
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| المؤلفون: | Tao Niu, Franklin Chi Meng Tay, Yang Jiao, Huan Liu, Ji Hua Chen |
| المصدر: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2019 (2019) |
| بيانات النشر: | Hindawi, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | 0301 basic medicine, Adult, Aging, Article Subject, Adolescent, NF-E2-Related Factor 2, Apoptosis, Oxidative phosphorylation, Mitochondrion, medicine.disease_cause, Protective Agents, Biochemistry, Models, Biological, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Coactivator, medicine, Humans, NRF1, lcsh:QH573-671, Dental Pulp, Activator (genetics), Chemistry, lcsh:Cytology, Nuclear Respiratory Factor 1, Intrinsic apoptosis, 030206 dentistry, Cell Biology, General Medicine, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Cell biology, Hydroquinones, Mitochondria, 030104 developmental biology, Methacrylates, Reactive Oxygen Species, Oxidative stress, Heme Oxygenase-1, Research Article |
| الوصف: | Dental resin monomers such as 2-hydroxyethyl methacrylate (HEMA) disturb vital cell functions and induce mitochondrial intrinsic apoptosis via generation of oxidative stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the gene expression of antioxidative enzymes and plays a crucial role in the maintenance of cellular redox equilibrium and mitochondrial homeostasis. The present study investigated the functional significance of Nrf2 in cellular response toward HEMA. It was found that HEMA stimulation promoted nuclear translocation of Nrf2 and increased Nrf2 and heme oxygenase-1 (HO-1) expression, which was further enhanced by Nrf2 activator tert-butylhydroquinone (tBHQ), but suppressed by Nrf2 inhibitor ML385. Pretreatment of primary human dental pulp cells (hDPCs) with tBHQ protected the cells from HEMA-induced oxidative injury (increased reactive oxygen species production and apoptosis) and mitochondrial impairment (morphological alterations, decreased ATP production, suppressed oxidative phosphorylation activity, depolarization of mitochondrial membrane potential, and disrupted electron transport chain). In contrast, pretreatment with ML385 increased cell sensitivity to these injurious processes. This protective effect on mitochondria could be related to peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α)/nuclear respiratory factor 1 (NRF1) pathway. These results contribute to the understanding of the function of Nrf2 and the development of novel therapies to counteract the adverse effects of dental resin monomers. |
| وصف الملف: | text/xhtml |
| اللغة: | English |
| تدمد: | 1942-0994 1942-0900 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a6ab92bc944fd6577fdbc67676a9b97aTest http://europepmc.org/articles/PMC6476051Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....a6ab92bc944fd6577fdbc67676a9b97a |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19420994 19420900 |
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