HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation
Background 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...
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oai:animorepository.dlsu.edu.ph:faculty_research-117352024-03-18T02:43:37Z HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation Marquez, Jubert Park, Nammi Garcia, Maria Victoria Faith Kim, Hyoung Kyu Han, Jin Background 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. Method 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. Results 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. Conclusion 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. 2020-01-01T08:00:00Z text https://animorepository.dlsu.edu.ph/faculty_research/11531 info:doi/10.1007/s13273-020-00090-w Faculty Research Work Animo Repository Resveratrol Mitochondria Oxidative stress Muscle cells Biology |
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Resveratrol Mitochondria Oxidative stress Muscle cells Biology Marquez, Jubert Park, Nammi Garcia, Maria Victoria Faith Kim, Hyoung Kyu Han, Jin HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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Background 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.
Method 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.
Results 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.
Conclusion 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. |
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Marquez, Jubert Park, Nammi Garcia, Maria Victoria Faith Kim, Hyoung Kyu Han, Jin |
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Marquez, Jubert Park, Nammi Garcia, Maria Victoria Faith Kim, Hyoung Kyu Han, Jin |
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Marquez, Jubert |
title |
HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
title_short |
HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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HS-1793 protects C2C12 cells from oxidative stress via mitochondrial function regulation |
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hs-1793 protects c2c12 cells from oxidative stress via mitochondrial function regulation |
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2020 |
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https://animorepository.dlsu.edu.ph/faculty_research/11531 |
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