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<p>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 (<i>P</i> &lt; 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.</p>

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Pea Peptides and Heavy Metal Neurotoxicity: Exploring Mechanisms and Mitigation Strategies in PC12 Cells

  • 期刊论文

  • 发表日期：

    2025年3月4日

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  • Ning Li,
  • Ningning Cui,
  • Tiange Li,
  • Peijun Zhao,
  • Ibrahim A. Bakry,
  • Qian Li,
  • Yongxia Cheng,
  • Gianni Galaverna,
  • Huijie Yang,
  • Fangyu Wang

摘要

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.