Ding Ling, Ye Hong, Gu Long-Dian, Du An-Qing, Yuan Xin-Lu
Department of Endocrinology and Metabolic Diseases, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Chin J Integr Med. 2022 Sep;28(9):809-816. doi: 10.1007/s11655-022-2893-4. Epub 2022 Jul 7.
To evaluate the effect of echinacoside (ECH) on cognitive dysfunction in post cerebral stroke model rats.
The post stroke cognitive impairment rat model was created by occlusion of the transient middle cerebral artery (MCAO). The rats were randomly divided into 3 groups by a random number table: the sham group (sham operation), the MCAO group (received operation for focal cerebral ischemia), and the ECH group (received operation for focal cerebral ischemia and ECH 50 mg/kg per day), with 6 rats in each group. The infarct volume and spatial learning were evaluated by triphenyl tetrazolium chloride staining and Morris water maze. The expression of α7nAChR in the hippocampus was detected by immunohistochemistry. The contents of acetylcholine (ACh), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), activities of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and catalase (CAT) were evaluated by enzyme linked immunosorbent assay. The neural apoptosis and autophagy were determined by TUNEL staining and LC3 staining, respectively.
ECH significantly lessened the brain infarct volume and ameliorated neurological deficit in infarct volume and water content (both P<0.01). Compared with MCAO rats, administration of ECH revealed shorter escape latency and long retention time at 7, 14 and 28 days (all P<0.01), increased the α7nAChR protein expression, ACh content, and ChAT activity, and decreased AChE activity in MCAO rats (all P<0.01). ECH significantly decreased MDA content and increased the GSH content, SOD, and CAT activities compared with MCAO rats (all P<0.05). ECH suppressed neuronal apoptosis by reducing TUNEL-positive cells and also enhanced autophagy in MCAO rats (all P<0.01).
ECH treatment helped improve cognitive impairment by attenuating neurological damage and enhancing autophagy in MCAO rats.
评估紫锥菊苷（ECH）对脑卒中小鼠模型认知功能障碍的影响。
通过短暂性大脑中动脉闭塞（MCAO）建立脑卒中后认知障碍大鼠模型。采用随机数字表法将大鼠随机分为3组：假手术组（假手术）、MCAO组（接受局灶性脑缺血手术）和ECH组（接受局灶性脑缺血手术且每天给予50 mg/kg ECH），每组6只大鼠。通过氯化三苯基四氮唑染色和Morris水迷宫评估梗死体积和空间学习能力。采用免疫组织化学法检测海马中α7nAChR的表达。通过酶联免疫吸附测定法评估乙酰胆碱（ACh）、丙二醛（MDA）、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）的含量，胆碱乙酰转移酶（ChAT）、乙酰胆碱酯酶（AChE）和过氧化氢酶（CAT）的活性。分别通过TUNEL染色和LC3染色测定神经细胞凋亡和自噬。
ECH显著减小脑梗死体积，改善梗死体积和含水量方面的神经功能缺损（均P<0.01）。与MCAO大鼠相比，给予ECH后在第7、14和28天的逃避潜伏期缩短，保留时间延长（均P<0.01），增加了MCAO大鼠中α7nAChR蛋白表达、ACh含量和ChAT活性，并降低了AChE活性（均P<0.01）。与MCAO大鼠相比，ECH显著降低MDA含量，增加GSH含量、SOD和CAT活性（均P<0.05）。ECH通过减少TUNEL阳性细胞抑制神经元凋亡，并增强MCAO大鼠的自噬（均P<0.01）。
ECH治疗通过减轻MCAO大鼠的神经损伤和增强自噬来帮助改善认知障碍。
