HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation
| العنوان: | HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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| المؤلفون: | Nammi Park, Jin Han, Hyoung Kyu Kim, Jubert Marquez, Maria Victoria Faith Garcia |
| المصدر: | Molecular & Cellular Toxicology. 16:359-365 |
| بيانات النشر: | Springer Science and Business Media LLC, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | 0301 basic medicine, Health, Toxicology and Mutagenesis, Mitochondrion, Toxicology, medicine.disease_cause, Pathology and Forensic Medicine, 03 medical and health sciences, 0302 clinical medicine, medicine, General Pharmacology, Toxicology and Pharmaceutics, PI3K/AKT/mTOR pathway, chemistry.chemical_classification, Reactive oxygen species, ATP synthase, biology, Public Health, Environmental and Occupational Health, Skeletal muscle, Cell biology, 030104 developmental biology, medicine.anatomical_structure, Mitochondrial biogenesis, chemistry, 030220 oncology & carcinogenesis, biology.protein, Phosphorylation, Oxidative stress |
| الوصف: | HS1793, a novel analogue of resveratrol, was previously determined to be more potent at lower dosages by improving mitochondrial function and increased mitochondrial biogenesis-related proteins. In this study, we focused on targeting the mitochondria to address muscle wasting with HS-1793. Dosage screening was performed by evaluating for cytotoxicity and cell proliferation. Mitochondrial mass, mitochondrial membrane potential (Δψm), reactive oxygen species (ROS) level, and mitochondria biogenesis-regulated genes and proteins were analyzed to determine the effects on mitochondrial biogenesis. HS-1793 reduced ROS generation, but treatment did not interfere with cellular viability at low dosages. HS-1793 also regulated mitochondrial function by increasing cellular and mitochondrial ATP synthesis function, stabilizing Δψm and decreasing ROS. More importantly, these dysfunction in these parameters were ameliorated by HS-1793 in a simulated oxidative stress model with tBHP. We also observed increase in mitochondrial mass and upregulation in vital mitochondrial biogenesis-related gene PGC1-α as a response to HS-1793 treatment. Moreover, phosphorylation of AKT and mTOR proteins, which are considered as regulators of skeletal muscle function were also increased during the treatment. Finally, HS-1793 also demonstrated protective effects against cisplatin-induced skeletal muscle cell injury by increasing expression of mitochondrial biogenesis-relate markers. Taken altogether, it shows the viability of HS-1793 as a compound that can restore mitochondrial function and render protection in skeletal muscle cells, especially during high oxidative stress levels. |
| تدمد: | 2092-8467 1738-642X |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::c0ef0827f8486e41e3b1b529048c6432 https://doi.org/10.1007/s13273-020-00090-w |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi...........c0ef0827f8486e41e3b1b529048c6432 |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 20928467 1738642X |
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