Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells
PI3K/mTOR/GSK3β pathway participates in the protective mechanism of emodin on H2O2-induced cell damage. SH-SY5Y cells were transfected with the PI3K inhibitor or GSK3β inhibitor, respectively, and treated with emodin at a concentration of 50 μM for 24 h and with H2O2 (200 μM) for 1 h. (a) The cell viability rate was determined using the MTT in each group. (b) The apoptosis rate (%) of SH-SY5Y in each group. (c) The level of IL-6, TNF-α, and NO of SH-SY5Y in each group. (d) The ROS level of SH-SY5Y in each group. (e) The NAD+ level of SH-SY5Y in each group. (f) The protein expression of cytochrome c of SH-SY5Y in each 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.
Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.