Acupoint catgut embedding attenuates oxidative stress and cognitive impairment in chronic cerebral ischemia by inhibiting the Ang II/AT1R/NOX axis

• Published in: Pflügers Archiv Vol. 476; no. 8; pp. 1249 - 1261
• Main Authors: Wei, Jurui, Ai, Qi, Lv, Peier, Fang, Wenyao, Wang, Zixuan, Zhao, Jiumei, Xu, Wenqing, Chen, Lin, Dong, Jun, Luo, Bijun
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.08.2024; Springer Nature B.V
• Subjects: Acupuncture; Acupuncture Points; Acupuncture Therapy - methods; Angiotensin II; Angiotensin II - metabolism; Animals; Biomedical and Life Sciences; Biomedicine; Brain Ischemia - metabolism; Catgut; Cell Biology; Cognitive ability; Cognitive Dysfunction - etiology; Cognitive Dysfunction - metabolism; Embedding; Enzyme-linked immunosorbent assay; Human Physiology; Immunohistochemistry; Ischemia; Male; Molecular Medicine; Molecular modelling; Neurological complications; Neuroprotection; Neuroscience; Neurosciences; Oxidative Stress; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1 - metabolism; Receptors; Western blotting; Oxidative stress; Chronic cerebral ischemia; Renin angiotensin system; Acupoint catgut embedding; Cognitive impairment
• ISSN: 0031-6768; 1432-2013; 1432-2013
• DOI: 10.1007/s00424-024-02981-6

Chronic cerebral ischemia (CCI) is a common neurological disorder, characterized by progressive cognitive impairment. Acupoint catgut embedding (ACE) represents a modern acupuncture form that has shown neuroprotective effects; nevertheless, its effects on CCI and the mechanisms remain largely unknown. Here, we aimed to explore the therapeutic action of ACE in CCI-induced cognitive impairment and its mechanisms. The cognitive function of CCI rats was determined using Morris water maze test, and histopathological changes in the brain were assessed through hematoxylin–eosin (HE) staining. To further explore the molecular mechanisms, the expression levels of oxidative stress markers and the Ang II/AT1R/NOX axis-associated molecules in the hippocampus were evaluated using enzyme-linked immunosorbent assay (ELISA), western blotting, and immunohistochemistry. Here, we observed that ACE treatment alleviated cognitive dysfunction and histopathological injury in CCI rats. Intriguingly, candesartan (an AT1R blocker) enhanced the beneficial effects of ACE on ameliorating cognitive impairment in CCI rats. Mechanistically, ACE treatment blocked the Ang II/AT1R/NOX pathway and subsequently suppressed oxidative stress, thus mitigating cognitive impairment in CCI. Our findings first reveal that ACE treatment could suppress cognitive impairment in CCI, which might be partly due to the suppression of Ang II/AT1R/NOX axis.