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颈动脉内膜切除术可改善临床和实验性单侧颈动脉狭窄中的认知障碍。

Carotid Endarterectomy Ameliorates Cognitive Impairment in Clinical and Experimental Unilateral Carotid Artery Stenosis.

作者信息

Cheng Yijun, Chen Bin, Zhang Miao, Chen Zhenghong, Liu Mingjian, Zhang Ziqian, Tang Hao, Wang Dapeng, Lv Wenwen, Li Biao, Dai Yuting, Shang Hanbing

机构信息

Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China.

Department of Neurosurgery, Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China.

出版信息

J Am Heart Assoc. 2025 Jan 21;14(2):e038388. doi: 10.1161/JAHA.124.038388. Epub 2025 Jan 16.

DOI:10.1161/JAHA.124.038388
PMID:39817552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12054441/
Abstract

BACKGROUND

Carotid endarterectomy (CEA) is widely used to treat carotid artery stenosis (CAS). However, the effects of CEA on unilateral CAS-induced cognitive impairment and the underlying mechanism remain poorly understood.

METHODS AND RESULTS

Thirteen patients diagnosed with unilateral severe CAS underwent pre- and post-CEA assessments, including fluoro-2-deoxy-d-glucose positron emission tomography/magnetic resonance imaging, cognitive assessments, and routine blood tests before and after CEA. Unilateral carotid common artery occlusion and ligation release (reperfusion) surgeries were performed in mice to mimic CAS and CEA. Cognitive function, cerebral blood flow, and white matter damage were evaluated in mice using the Morris water maze test, Doppler flowmetry, laser-speckle imaging, diffusion tensor imaging, Luxol fast blue staining, transmission electron microscopy, and western blot assays post unilateral carotid common artery occlusion and reperfusion. Genomic sequencing of the white matter was performed to explore the potential underlying mechanism. CEA significantly enhanced the Montreal Cognitive Assessment scores in patients with CAS and preoperative cognitive impairment. Moreover, CEA led to notable improvements in cerebral blood flow, energy metabolism, and white matter integrity, while concurrently reducing blood inflammation. In the mouse model, reperfusion surgery alleviated cognitive deficits, increased cerebral blood flow, and alleviated white matter damage following unilateral carotid common artery occlusion. Furthermore, transcriptional surveys have revealed substantial alterations in the upregulation of Nrf2 signaling and metabolic pathways, coupled with the inhibition of neuroinflammation, cellular communication, and immune cell population signaling following reperfusion.

CONCLUSIONS

CEA ameliorated CAS-induced cognitive dysfunction by improving the cerebral functional structure. These beneficial effects may be attributed to their antioxidant and anti-inflammatory properties.

摘要

背景

颈动脉内膜切除术(CEA)被广泛用于治疗颈动脉狭窄(CAS)。然而,CEA对单侧CAS所致认知障碍的影响及其潜在机制仍知之甚少。

方法与结果

13例诊断为单侧严重CAS的患者在CEA术前和术后接受了评估,包括氟代脱氧葡萄糖正电子发射断层扫描/磁共振成像、认知评估以及CEA术前和术后的常规血液检查。在小鼠身上进行单侧颈总动脉闭塞和结扎释放(再灌注)手术以模拟CAS和CEA。在单侧颈总动脉闭塞和再灌注后,使用莫里斯水迷宫试验、多普勒血流仪、激光散斑成像、扩散张量成像、Luxol固蓝染色、透射电子显微镜和蛋白质印迹分析对小鼠的认知功能、脑血流量和白质损伤进行评估。对白质进行基因组测序以探索潜在的潜在机制。CEA显著提高了患有CAS和术前认知障碍患者的蒙特利尔认知评估得分。此外,CEA导致脑血流量、能量代谢和白质完整性显著改善,同时减少血液炎症。在小鼠模型中,再灌注手术减轻了单侧颈总动脉闭塞后的认知缺陷,增加了脑血流量,并减轻了白质损伤。此外,转录调查显示,再灌注后Nrf2信号通路和代谢途径上调,同时神经炎症、细胞通讯和免疫细胞群体信号受到抑制,发生了实质性改变。

结论

CEA通过改善脑功能结构改善了CAS所致的认知功能障碍。这些有益作用可能归因于其抗氧化和抗炎特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/29cb34bf31f1/JAH3-14-e038388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/90a544a490dc/JAH3-14-e038388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/b4a33214ef20/JAH3-14-e038388-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/28285955cfb8/JAH3-14-e038388-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/bc26a3d236be/JAH3-14-e038388-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/7aaa6e4b05c2/JAH3-14-e038388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/29cb34bf31f1/JAH3-14-e038388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/90a544a490dc/JAH3-14-e038388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/b4a33214ef20/JAH3-14-e038388-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/28285955cfb8/JAH3-14-e038388-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/bc26a3d236be/JAH3-14-e038388-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/7aaa6e4b05c2/JAH3-14-e038388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f3b/12054441/29cb34bf31f1/JAH3-14-e038388-g001.jpg

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