Department of Rehabilitation, The First People's Hospital of Hangzhou Lin'an District, No.360 YiKang Street, Hangzhou, 311300, China.
Science and Education Section, The First People's Hospital of Hangzhou Lin'an District, Hangzhou, 311300, China.
Pflugers Arch. 2024 Aug;476(8):1249-1261. doi: 10.1007/s00424-024-02981-6. Epub 2024 Jun 28.
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.
慢性脑缺血（CCI）是一种常见的神经系统疾病，其特征是进行性认知障碍。穴位埋线（ACE）是一种现代针灸形式，具有神经保护作用；然而，其对 CCI 的作用及其机制在很大程度上尚不清楚。在这里，我们旨在探讨 ACE 在 CCI 诱导的认知障碍中的治疗作用及其机制。通过 Morris 水迷宫试验确定 CCI 大鼠的认知功能，并通过苏木精-伊红（HE）染色评估大脑的组织病理学变化。为了进一步探讨分子机制，使用酶联免疫吸附试验（ELISA）、Western blot 和免疫组织化学评估海马中氧化应激标志物和 Ang II/AT1R/NOX 轴相关分子的表达水平。在这里，我们观察到 ACE 治疗减轻了 CCI 大鼠的认知功能障碍和组织病理学损伤。有趣的是，坎地沙坦（AT1R 阻断剂）增强了 ACE 对改善 CCI 大鼠认知障碍的有益作用。机制上，ACE 治疗阻断了 Ang II/AT1R/NOX 通路，随后抑制了氧化应激，从而减轻了 CCI 大鼠的认知障碍。我们的研究结果首次揭示，ACE 治疗可以抑制 CCI 大鼠的认知障碍，这可能部分是由于抑制了 Ang II/AT1R/NOX 轴。
