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Further studies revealed that DAA was able to bind to Keap1 in the cytoplasm and increase the luciferase activity of Nrf2-antioxidant reactive element (ARE), promoting the expression of downstream antioxidant gene hame oxygenase-1 (HO-1), GSH, and GPx4 through the Keap1/Nrf2 pathway, while DAA treatment results in achieving attenuation of ROS and lipid peroxidation (36)
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This supports better muscle recovery and reduces the deep, aching pain that often accompanies even minimal physical activity in chronic illness
Histological analysis via H&E staining further showed that GPX4 knockdown partially abrogated the protective effects of TA (Figure 5C)
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