Gold nanoparticles reduce ischemic brain injury in rats by activating autophagy and inhibiting apoptosis

IF 2.6 4区医学 Q3 NEUROSCIENCES

Brain Research Pub Date : 2025-09-30 DOI:10.1016/j.brainres.2025.149974

Xuejing Ma, Chang Liu, Yanyan Yang, Lili Ren, Yunhao Xu, Jiachen Li, Peng Wang

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Abstract

Ischemic stroke, the main type of stroke, is the leading cause of human death and disability worldwide. This study aims to investigate the effect of gold nanoparticles (Au-NPs) on cerebral ischemia/reperfusion (I/R) injury in rats. Au-NPs was prepared by trisodium citrate reduction method. Transient middle cerebral artery occlusion/reperfusion (tMCAO) was used to mimic cerebral ischemia. Behavioral tests, 2,3,5-triphenyl tetrazolium chloride staining, Hematoxylin & Eosin staining, Nissl staining and TUNEL staining, were performed to evaluate cerebral injury following tMCAO. Brain tissues were collected and analyzed for ERK activation, autophagy, and apoptosis. The particle size of the prepared Au-NPs was about 15 nm, and the distribution was regular and uniform. Au-NPs treatment improved neurological outcomes and reduced infarct volume. Furthermore, Au-NPs treatment alleviated tMCAO induced apoptosis in rats and increased autophagy. In addition, Au-NPs treatment activated the ERK and ERK inhibitor PD98059 reversed the neuroprotective effects of Au-NPs on ischemic stroke injury.

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金纳米颗粒通过激活自噬和抑制细胞凋亡减少大鼠缺血性脑损伤。

缺血性中风是中风的主要类型，是全世界人类死亡和残疾的主要原因。本研究旨在探讨金纳米颗粒（Au-NPs）对大鼠脑缺血再灌注（I/R）损伤的影响。采用柠檬酸三钠还原法制备Au-NPs。短暂性大脑中动脉闭塞/再灌注（tMCAO）模拟脑缺血。行为学测试、2,3,5-三苯四氮氯化铵染色、苏木精和伊红染色、尼索染色和TUNEL染色评价tMCAO后的脑损伤。收集脑组织并分析ERK活化、自噬和凋亡。制备的Au-NPs粒径约为15 nm，分布规则均匀。Au-NPs治疗改善了神经预后并减少了梗死体积。此外，Au-NPs处理可减轻tMCAO诱导的大鼠细胞凋亡，增加自噬。此外，Au-NPs治疗激活ERK和ERK抑制剂PD98059逆转了Au-NPs对缺血性脑卒中损伤的神经保护作用。

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来源期刊

Brain Research 医学-神经科学

CiteScore

5.90

自引率

3.40%

发文量

268

审稿时长

47 days

期刊介绍： An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.