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Black soybean peptide mediates the AMPK/SIRT1/NF-κB signaling pathway to alleviate Alzheimer's-related neuroinflammation in lead-exposed HT22 cells

文献类型： 外文期刊

作者： Yang, Huijie 1 ; Wang, Fangyu 2 ; Zhao, Peijun 1 ; Ullah, Saif 1 ; Ma, Yan 1 ; Zhao, Guangshan 1 ; Cheng, Yongxia 1 ; Li, Qian 1 ; Li, Tiange 1 ; Qiao, Mingwu 1 ; Song, Lianjun 1 ; Zhang, Lei 1 ; Galaverna, Gianni 3 ; Huang, Xianqing 1 ; Li, Ning 1 ;

作者机构： 1.Henan Agr Univ, Coll Food Sci & Technol, 63 Agr Rd, Zhengzhou 450000, Peoples R China

2.Henan Acad Agr Sci, Key Lab Anim Immunol, 116 Huayuan Rd, Zhengzhou 450002, Peoples R China

3.Univ Parma, Food & Drug Dept, Parco Area Sci 17-a, I-43124 Parma, Italy

关键词： Black soybean peptide; Lead (Pb); Alzheimer's disease; Neuroinflammation; AMPK/SIRT1/NF-kappa B pathway

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.5； 五年影响因子：8.7 ）

ISSN： 0141-8130

年卷期： 2025 年 286 卷

页码：

收录情况： SCI

摘要： Alzheimer's disease (AD) is a neurodegenerative disorder characterized by hyperphosphorylation of tau, neuroinflammation, and amyloid-beta (A(3) 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 A(31-42 deposition. In addition, BSP1 effectively alleviated Pb-induced neuroinflammation by reducing the phosphorylation of NF-kappa B and the expression of pro-inflammatory cytokines (IL-1(3, TNF-alpha, 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 Pbinduced neuroinflammation.

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