• Xuan Zhang, Wenjie Xu, Huan Li, Dapeng Ruan, Siyuan Chen, Na Chu, Quan Zhen, and Yun Wang.
• School of Public Health, Bengbu Medical College, Bengbu, Anhui, China.
• Medicine (Baltimore). 2024 Nov 1; 103 (44): e40372e40372.

AbstractCadmium (Cd) is an environmental pollutant that can cause neurodegenerative disorders. Luteolin (Lut) is a natural flavonoid compound. However, whether Lut protects against Cd-induced nerve cell death remains unclear. In the present study, PC12 cells were used to investigate the neuroprotective effect of Lut against Cd poisoning. Changes in cell viability, apoptosis, B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein expression, and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway activity were analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Hoechst 33258 staining, flow cytometry, and western blotting. Lut markedly attenuated the Cd-induced reduction in cell viability, nuclear fragmentation, condensation, and the decrease in the Bcl-2/Bcl-2-associated X protein ratio in PC12 cells. Furthermore, Lut blocked the Cd-mediated activation of the Akt/mTOR signaling pathway. Moreover, inhibition of the Akt/mTOR signaling pathway with LY294002 (a PI3K inhibitor) enhanced the protective effect of Lut against Cd-induced cell death by suppressing Cd-induced activation of Akt, mTOR, and eukaryotic initiation factor 4E binding protein 1. The results showed that Lut prevented Cd-induced cell death partly by blocking the Akt/mTOR signaling pathway. Lut may be a potential agent for preventing Cd-induced nerve cell damage and neurodegenerative diseases.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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