Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells

Figure 3

Emodin alleviated mitochondrial dysfunction and oxidative stress of H₂O₂-induced neuroblastoma cell SH-SY5Y. SH-SY5Y cells were treated with emodin at a concentration of 50 μM for 24 h and with H₂O₂ (200 μM) for 1 h. The experiment was divided into the control group, H₂O₂ group, and H₂O₂+emodin group. (a) The ROS level in the control group, H₂O₂ group, and H₂O₂+emodin group. (b) The NAD⁺ level in the control group, H₂O₂ group, and H₂O₂+emodin group. (c) The ATP level in the control group, H₂O₂ group, and H₂O₂+emodin group. (d) Mitochondrial membrane potential measured by JC-1. (e) The protein expression of cytochrome c in the control group, H₂O₂ group, and H₂O₂+emodin group. “” means compared with the untreated group at , and “#” means compared with the H₂O₂ group at . GAPDH was used as an invariant internal control for calculating protein fold changes.

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