Lead (Pb) exposure poses significant health risks, particularly in neurodegenerative diseases such as Alzheimer's disease (AD). This study investigates the neuroprotective effects of pea peptide (PP4) Show more
Lead (Pb) exposure poses significant health risks, particularly in neurodegenerative diseases such as Alzheimer's disease (AD). This study investigates the neuroprotective effects of pea peptide (PP4) on PC12 cells exposed to Pb. Using Cell Counting Kit-8 (CCK-8), pretreatment with PP4 at 50 and 200 µM concentrations significantly improved cell viability compared to Pb-only treated cells (P < 0.05), indicating a protective effect. Moreover, Pb exposure led to increased Amyloid Precursor Protein (APP) expression at 10 and 20 µM after 24 h (P < 0.05), while β-site amyloid Precursor Protein Cleaving Enzyme 1 (BACE1) levels were elevated across all concentrations tested (P < 0.05). We established that PP4 can mitigate Pb-induced cytotoxicity and reduce the expression of APP and BACE1 by activating the Phosphoinositide 3-kinase / Protein Kinase (PI3K/AKT) signaling pathway. This study highlights the potential of PP4 as a therapeutic agent in preventing neurotoxic damage associated with lead exposure, suggesting a novel approach for the management of AD. Show less
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by hyperphosphorylation of tau, neuroinflammation, and amyloid-beta (Aβ) plaques. Lead (Pb) exposure has been linked to an increa Show more
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by hyperphosphorylation of tau, neuroinflammation, and amyloid-beta (Aβ) plaques. Lead (Pb) exposure has been linked to an increased risk of AD and neuroinflammation. The purpose of this study is to determine if black soybean peptide (BSP1) may reduce neuroinflammation caused by Pb and associated AD-like pathology. Pb exposure was given to mouse hippocampus HT22 cells in the presence or absence of BSP1, positive control resveratrol (Rsv), or the SIRT1 inhibitor EX-527. Our findings suggest that BSP1 downregulates the expression of beta-secretase (BACE1) and amyloid precursor protein (APP), inhibits tau phosphorylation, and reduces Aβ1-42 deposition. In addition, BSP1 effectively alleviated Pb-induced neuroinflammation by reducing the phosphorylation of NF-κB and the expression of pro-inflammatory cytokines (IL-1β, TNF-α, NLRP3, and IL-18). BSP1 provides neuroprotective effect via phosphorylating LKB1 and AMPK, inhibiting mTOR signaling, and activating the AMPK/SIRT1 pathway. These results suggest that BSP1 may be therapeutically beneficial for preventing or treating AD by reducing Pb-induced neuroinflammation. Show less