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<p>Lead (Pb) exposure is a major environmental risk factor for neurodegenerative diseases. This study investigates the neuroprotective effects of black soybean peptides (BSPs), particularly BSP1, BSP3, and BSP4, against Pb-induced toxicity in HT22 mouse hippocampal neuron cells, with a mechanistic focus on the RhoA/MAPK signaling pathway. The rationale for targeting RhoA/MAPK stems from their established roles in mediating oxidative stress and apoptosis in Pb-related pathology. Pretreatment with BSP1 or BSP4 (200&#xa0;µM) increased cell viability by approximately 35% relative to the Pb-only group. At the same time, BSPs also decreased intracellular reactive oxygen species (ROS) levels by up to 40% and malondialdehyde (MDA) by 30%. Antioxidant enzyme activities, including superoxide dismutase (SOD) and catalase (CAT), were restored to near-control levels; for example, SOD activity increased 1.8-fold compared with the Pb group. Western blot and immunofluorescence confirmed that BSPs reduced the Pb-triggered activation of RhoA, ROCK1/2, and MAPK proteins (p38, JNK, ERK). These findings demonstrate that BSPs mitigate Pb-induced neurotoxicity by enhancing antioxidant activity and targeting RhoA/MAPK signaling, highlighting their potential as functional food ingredients or therapeutic agents for neuroprotection. </p>

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Black Soybean Peptides Attenuate Lead-Induced Neurotoxicity: Role of Oxidative Stress and the RhoA/MAPK Signaling Pathway

  • 期刊论文

  • 发表日期：

    2025年11月28日

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  • Huijie Yang,
  • Fangyu Wang,
  • Qian Li,
  • Tiange Li,
  • Bei Zhang,
  • Lianjun Song,
  • Xianqing Huang,
  • Shuyang Liu,
  • Gianni Galaverna,
  • Peijun Zhao,
  • Ibrahim A. Bakry,
  • Ning Li

摘要

Lead (Pb) exposure is a major environmental risk factor for neurodegenerative diseases. This study investigates the neuroprotective effects of black soybean peptides (BSPs), particularly BSP1, BSP3, and BSP4, against Pb-induced toxicity in HT22 mouse hippocampal neuron cells, with a mechanistic focus on the RhoA/MAPK signaling pathway. The rationale for targeting RhoA/MAPK stems from their established roles in mediating oxidative stress and apoptosis in Pb-related pathology. Pretreatment with BSP1 or BSP4 (200 µM) increased cell viability by approximately 35% relative to the Pb-only group. At the same time, BSPs also decreased intracellular reactive oxygen species (ROS) levels by up to 40% and malondialdehyde (MDA) by 30%. Antioxidant enzyme activities, including superoxide dismutase (SOD) and catalase (CAT), were restored to near-control levels; for example, SOD activity increased 1.8-fold compared with the Pb group. Western blot and immunofluorescence confirmed that BSPs reduced the Pb-triggered activation of RhoA, ROCK1/2, and MAPK proteins (p38, JNK, ERK). These findings demonstrate that BSPs mitigate Pb-induced neurotoxicity by enhancing antioxidant activity and targeting RhoA/MAPK signaling, highlighting their potential as functional food ingredients or therapeutic agents for neuroprotection.