电针通过PI3K/AKT信号通路改善大鼠蛛网膜下腔出血后的认知障碍。
Electroacupuncture improves cognitive impairment after subarachnoid hemorrhage in rats through the PI3K/AKT signaling pathway.
作者信息
Zhou Feng, Wang Zhenzhi, Xiong Kang, Fu Xiaoman, Jiang Hongru, Zhang Meiling, Wang Qiang, Wang Yuan
机构信息
Department of Neurosurgery, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, China.
Department of Chinese and Western Medicine, Shaanxi University of Chinese Medicine, Xianyang, China.
出版信息
Acupunct Med. 2025 Feb;43(1):26-37. doi: 10.1177/09645284251314187. Epub 2025 Jan 31.
OBJECTIVE
Cognitive impairment (CI) is highly prevalent in subarachnoid hemorrhage (SAH) patients. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays a critical role in neuronal survival in a variety of central nervous system injuries. This study aimed to determine whether electroacupuncture (EA) at and LI20 ameliorates SAH-CI in a rat model and to examine whether it modulates the PI3K/AKT pathway by administering a PI3K inhibitor (LY294002) versus dimethyl sulfoxide (DMSO) vehicle.
METHODS
Notably, 129 male Sprague-Dawley rats were divided into Blank, Sham, SAH and SAH + EA groups (Experiment 1, = 54) and SAH, SAH + EA, SAH + LY294002, SAH + EA + LY294002 and SAH + EA + DMSO groups (Experiment 2, = 75). Garcia scoring was used to evaluate neurological function. The moisture content of the rat brain was determined by dry‒wet method. The Morris water maze was used to assess learning and memory function. Pathological changes in neurons in the hippocampus were observed via hematoxylin-eosin (H&E) staining. The number of surviving neurons and the percentage of apoptotic cells in the hippocampus were detected via Nissl and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. The expression of PI3K/AKT pathway-related proteins was detected via Western blotting.
RESULTS
The results indicated that EA intervention after SAH reduced brain water content, enhanced Garcia scores, improved neurological function and behavioral markers of CI, and increased the number of surviving neurons in the hippocampus. Moreover, EA significantly increased the expression of AKT, phosphorylated (p)-AKT, PI3K, p-PI3K, glycogen synthase kinase (GSK)-3β, p-GSK-3β and B cell lymphoma (Bcl)-2 proteins, and decreased the expression of Bcl-2-associated X (Bax) and caspase-3. In addition, the effects of EA were abolished by LY294002.
CONCLUSION
EA appeared to improve CI in a rat model of SAH through the activation of the PI3K/AKT pathway.
目的
认知障碍（CI）在蛛网膜下腔出血（SAH）患者中高度普遍。磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（AKT）信号通路在多种中枢神经系统损伤的神经元存活中起关键作用。本研究旨在确定针刺双侧百会穴（GV20）和双侧迎香穴（LI20）是否能改善SAH大鼠模型中的SAH-CI，并通过给予PI3K抑制剂（LY294002）与二甲基亚砜（DMSO）溶剂对照，研究其是否通过调节PI3K/AKT信号通路发挥作用。
方法
值得注意的是，将129只雄性Sprague-Dawley大鼠分为空白组、假手术组、SAH组和SAH+电针组（实验1，n = 54），以及SAH组、SAH+电针组、SAH+LY294002组、SAH+电针+LY294002组和SAH+电针+DMSO组（实验2，n = 75）。采用Garcia评分评估神经功能。采用干湿法测定大鼠脑含水量。采用Morris水迷宫评估学习记忆功能。通过苏木精-伊红（H&E）染色观察海马神经元的病理变化。通过尼氏染色和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）染色检测海马中存活神经元的数量和凋亡细胞的百分比。通过蛋白质印迹法检测PI3K/AKT信号通路相关蛋白的表达。
结果
结果表明，SAH后电针干预可降低脑含水量，提高Garcia评分，改善CI的神经功能和行为指标，并增加海马中存活神经元的数量。此外，电针显著增加AKT、磷酸化（p）-AKT、PI3K、p-PI3K、糖原合酶激酶（GSK）-3β、p-GSK-3β和B细胞淋巴瘤（Bcl）-2蛋白的表达，并降低Bcl-2相关X蛋白（Bax）和半胱天冬酶-3的表达。此外，LY294002消除了电针的作用。
结论
电针可能通过激活PI3K/AKT信号通路改善SAH大鼠模型中的CI。
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