Ameliorative Mechanism of Malvidin-3-O-glucoside on Chlorpyrifos-Induced PC12 Cell Injury

This study aimed to investigate the protective effects and underlying mechanisms of malvidin-3-O-glucoside (Mv3G) on chlorpyrifos-induced damage of PC12 cells. The optimal dose of chlorpyrifos for inducing cell injury and the optimal dose of Mv3G for protecting against cell injury were determined. Western blot analysis was used to observe the changes in the expression of phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway-related proteins, the autophagy-related protein Beclin1, and mammalian target of rapamycin (mTOR) following Mv3G treatment. The levels of the oxidative stress biomarker glutathione (GSH), the inflammatory cytokine tumor necrosis factor-α (TNF-α), acetylcholine esterase (AChE) activity, and the apoptosis-related protein cysteineaspartic protease-3 (Caspase-3) were measured using enzyme-linked immunosorbent assay. Based on cell viability and morphological changes, the optimal chlorpyrifos concentration was 30 µmol/L, and the optimal Mv3G concentration was 200 µmol/L. Experimental results demonstrated that Mv3G significantly improved the survival rate of chlorpyrifos-damaged PC12 cells, alleviated the inhibitory effect of chlorpyrifos on the PI3K/AKT signaling pathway, and increased GSH levels and AChE activity while reducing TNF-α levels and the expression of Beclin1 and Caspase-3. These findings indicate that Mv3G mitigates chlorpyrifos-induced oxidative stress, neuroinflammation, cholinergic dysfunction, apoptosis, and abnormal autophagy through the PI3K/AKT signaling pathway.