Neuroprotective effects of traditional Chinese medicine Naofucong on diabetic cognitive impairment: Mechanisms involving insulin-degrading enzyme-mediated degradation of Amyloid-(3 and inhibition of ERK/JNK/ p38 MAPK signaling pathway

被引：1

作者：

Tian, Yue ^{[1
]}

Jing, Guangchan ^{[1
]}

Yin, Ruiying ^{[1
]}

Ma, Mei ^{[1
]}

Cao, Weiwei ^{[2
]}

Zhang, Mengren ^{[1
]}

机构：

[1] Peking Union Med Coll & Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Tradit Chinese Med, 1 Shuaifuyuan, Beijing 100730, Peoples R China

[2] Beijing HFK Biosci Co LTD, Beijing 102200, Peoples R China

来源：

BRAIN RESEARCH | 2025年 / 1849卷

关键词：

Diabetic cognitive impairment; Insulin-degrading enzyme; Amyloid-(3; Phosphorylated Tau; Mitogen-activated protein kinases; Oxidative stress; ALZHEIMERS-DISEASE; BETA; MEMORY; DYSFUNCTION; BRAIN;

D O I：

10.1016/j.brainres.2024.149365

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The increasing prevalence of diabetes and its related cognitive impairments is a significant public health concern. With limited clinical treatment options and an incomplete understanding of the underlying mechanisms, traditional Chinese medicine (TCM) Naofucong is proposed as a potential neuroprotective agent against diabetic cognitive impairment (DCI). This study aims to investigate the therapeutic mechanisms of Naofucong in DCI. We hypothesize that Naofucong may improve cognitive function in diabetic rats by modulating the extracellular regulated protein kinases (ERK)/c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinases (MAPK) signaling pathway, enhancing insulin-degrading enzyme (IDE) expression, reducing amyloid-beta (A(3) deposition, decreasing phosphorylated Tau (p-Tau) levels, and alleviating oxidative stress. Diabetes was induced in specific-pathogen-free male Sprague-Dawley rats using streptozotocin, and the rats were treated with oral Naofucong for 12 weeks. We assessed cognitive function and measured neuronal damage, oxidative stress injury, and the expression levels of IDE, A(3, amyloid precursor protein (APP), p-Tau, and components of the ERK/JNK/ p38 MAPK pathway. Diabetic rats showed significant declines in cognitive function, neuronal damage, oxidative stress, low IDE expression, A(3 accumulation, high APP expression, abnormal Tau phosphorylation, and overactivation of the ERK/JNK/p38 MAPK pathway. Naofucong treatment significantly reversed these symptoms. Our findings suggest that Naofucong improves cognitive impairment in diabetic rats by inhibiting the ERK/JNK/ p38 MAPK pathway, upregulating IDE, reducing A(3 deposition, suppressing APP and p-Tau expression, and alleviating neuronal damage and oxidative stress. This research provides a reference for the clinical prevention and treatment of DCI using TCM Naofucong.

引用

页数：20