豌豆肽与重金属神经毒性：探索PC12细胞中的作用机制及缓解策略
Pea Peptides and Heavy Metal Neurotoxicity: Exploring Mechanisms and Mitigation Strategies in PC12 Cells.
作者信息
Li Ning, Cui Ningning, Li Tiange, Zhao Peijun, Bakry Ibrahim A, Li Qian, Cheng Yongxia, Galaverna Gianni, Yang Huijie, Wang Fangyu
机构信息
College of Food Science and Technology, Henan Agricultural University, 63# Agricultural Road, Zhengzhou, 450000, China.
Key Laboratory for Animal Immunology, Henan Academy of Agricultural Sciences, 116# Huayuan Road, Zhengzhou, 450002, PR China.
出版信息
Plant Foods Hum Nutr. 2025 Mar 4;80(1):85. doi: 10.1007/s11130-025-01322-x.
Calsyntenin-1 (Clst1) is a sensitive indicator of lead (Pb) toxicity in neural tissue. This study was designed to investigate the impact of lead exposure on Clst1 expression in PC12 cells and the mitigating effect of pea peptide 4 (PP4) on lead-induced neurotoxicity. Data showed that lead exposure, at varying doses and durations, disrupted the mRNA expression and protein levels of Clstn1 in PC12 cells. However, immunofluorescence results showed that treatment with PP4 significantly increased Clstn1 protein expression in the Pb + PP4 and PP4 groups compared to the Pb groups (P < 0.05). Lead exposure activates the JNK and p38 pathways; at the same time, PP4 treatment enhances ERK pathway activation and reduces JNK and p38 activation.
钙黏连蛋白-1（Clst1）是神经组织中铅（Pb）毒性的敏感指标。本研究旨在探讨铅暴露对PC12细胞中Clst1表达的影响以及豌豆肽4（PP4）对铅诱导的神经毒性的缓解作用。数据显示，不同剂量和持续时间的铅暴露会破坏PC12细胞中Clstn1的mRNA表达和蛋白质水平。然而，免疫荧光结果显示，与铅处理组相比，PP4处理显著增加了铅+PP4组和PP4组中Clstn1蛋白的表达（P<0.05）。铅暴露会激活JNK和p38信号通路；同时，PP4处理增强了ERK信号通路的激活，并降低了JNK和p38的激活。
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