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

IF 2.9 4区 医学 Q2 PHYSIOLOGY Pflugers Archiv : European journal of physiology Pub Date : 2024-08-01 Epub Date: 2024-06-28 DOI:10.1007/s00424-024-02981-6
Jurui Wei, Qi Ai, Peier Lv, Wenyao Fang, Zixuan Wang, Jiumei Zhao, Wenqing Xu, Lin Chen, Jun Dong, Bijun Luo
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Abstract

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.

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穴位猫肠草包埋通过抑制Ang II/AT1R/NOX轴减轻慢性脑缺血的氧化应激和认知障碍
慢性脑缺血(CCI)是一种常见的神经系统疾病,以进行性认知功能障碍为特征。穴位鲇鱼嵌(ACE)是一种现代针灸形式,具有神经保护作用;然而,它对 CCI 的影响及其机制在很大程度上仍不为人所知。在此,我们旨在探讨穴位埋线对 CCI 引起的认知障碍的治疗作用及其机制。我们利用莫里斯水迷宫试验测定了CCI大鼠的认知功能,并通过苏木精-伊红(HE)染色评估了脑组织病理学变化。为了进一步探讨分子机制,我们使用酶联免疫吸附试验(ELISA)、Western 印迹和免疫组织化学方法评估了氧化应激标志物和 Ang II/AT1R/NOX 轴相关分子在海马中的表达水平。在这里,我们观察到 ACE 治疗缓解了 CCI 大鼠的认知功能障碍和组织病理学损伤。耐人寻味的是,坎地沙坦(一种 AT1R 阻断剂)增强了 ACE 对改善 CCI 大鼠认知功能障碍的有益作用。从机理上讲,ACE治疗阻断了Ang II/AT1R/NOX通路,继而抑制了氧化应激,从而减轻了CCI大鼠的认知损伤。我们的研究结果首次揭示了 ACE 治疗可抑制 CCI 大鼠的认知损伤,这可能部分归因于 Ang II/AT1R/NOX 轴的抑制作用。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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