ArticleMolecular neurobiology2025
Black Soybean Peptides Attenuate Lead-Induced Neurotoxicity: Role of Oxidative Stress and the RhoA/MAPK Signaling Pathway.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
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.
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