Black Bean Peptide Alleviates Lead-Induced Hippocampal Neurotoxicity in Mice by Regulating PINK1/Parkin-Mediated Mitophagy.

Authors

Jiawen Sun, Qian Li, Tiange Li, Xing Li, Xianqing Huang, Yongxia Cheng, Guangshan Zhao, Lianjun Song, Mingwu Qiao, Gianni Galaverna, Peijun Zhao, Ning Li

Published in

Journal of food science. Volume 91. Issue 6. Pages e71233.

Abstract

Lead (Pb) exposure is a major environmental risk factor for cognitive impairment. This effect is mainly caused by oxidative stress, mitochondrial dysfunction in the hippocampus, and neuronal apoptosis. This study examined whether black bean peptide (BSP) reduces Pb-induced hippocampal neurotoxicity by regulating PINK1/Parkin-mediated mitophagy. A mouse model of Pb exposure was established by oral gavage. The effects of BSP were assessed using biochemical assays, Western blot, immunofluorescence, and molecular docking. Results showed that BSP significantly increased total antioxidant capacity (T-AOC) and restored the activities of superoxide dismutase (SOD) and catalase (CAT). PINK1/Parkin-dependent mitophagy was activated, as shown by increased levels of PINK1, Parkin, and LC3B-II and decreased p62 accumulation. BSP also significantly inhibited Pb-induced neuronal apoptosis. This was demonstrated by reduced expression of BCL2-associated X protein (Bax) and cysteine-aspartic acid protease 3 (Caspase-3) and increased expression of B-cell lymphoma 2 (Bcl-2) (p < 0.05). Molecular docking predicted a binding free energy of -6.9 kcal/mol for the BSP-PINK1 complex, indicative of a moderate and thermodynamically favorable interaction that may underpin its neuroprotective effect. No significant difference was found between the BSP (200 mg/kg/day) and resveratrol (RSV, 80 mg/kg/day) groups (p > 0.05). In conclusion, these results suggest that BSP improves mitochondrial quality control, reduces oxidative damage, and inhibits apoptosis in a mouse model of Pb-induced neurotoxicity, highlighting its potential as a candidate dietary strategy for further investigation in the context of heavy metal-related cognitive decline.

PMID:
42324632
Bibliographic data and abstract were imported from PubMed on 22 Jun 2026.

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