刘福德,于 嘉,王建懿,陈 晨,方 伟.丁苯酞对颈动脉狭窄大鼠认知功能及海马CA1区神经元凋亡的影响及相关机制研究[J].现代生物医学进展英文版,2022,(13):2411-2415. |
丁苯酞对颈动脉狭窄大鼠认知功能及海马CA1区神经元凋亡的影响及相关机制研究 |
Effects of Butylphthalide on Cognitive Function and Neuronal Apoptosis in Hippocampal CA1 Area of Rats with Carotid Artery Stenosis and Related Mechanisms |
Received:November 05, 2021 Revised:November 30, 2021 |
DOI:10.13241/j.cnki.pmb.2022.13.002 |
中文关键词: 剂量 丁苯酞 颈动脉狭窄 海马CA1区 神经元凋亡 氧化应激 认知功能 |
英文关键词: Dose Butylphthalide Carotid artery stenosis Hippocampal CA1 area Neuronal apoptosis Oxidative stress Cognitive function |
基金项目:陕西省重点研发计划项目(2021SF-059) |
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中文摘要: |
摘要 目的:探讨与研究丁苯酞对颈动脉狭窄大鼠认知功能及海马CA1区神经元凋亡的影响及相关机制。方法:将颈动脉狭窄大鼠大鼠(n=42)随机为三组-模型组、低剂量丁苯酞(20 mg/kg)组和高剂量丁苯酞(40 mg/kg)组,每组14只。低剂量丁苯酞组与高剂量丁苯酞组每天给予20 mg/kg、40 mg/kg丁苯酞灌胃治疗,对照组给予等剂量的生理盐水灌胃,持续21 d。结果:低剂量丁苯酞组与高剂量丁苯酞组治疗第7 d、第14 d、第21 d的BBT评分低于模型组(P<0.05),高剂量丁苯酞组低于低剂量丁苯酞组(P<0.05)。低剂量丁苯酞组与高剂量丁苯酞组治疗第21 d、第28 d的海马CA1区神经元凋亡指数低于模型组,高剂量丁苯酞组低于低剂量丁苯酞组(P<0.05)。低剂量丁苯酞组与高剂量丁苯酞组治疗第21 d、第28 d的脑组织超氧化物歧化酶(Superoxide dismutase,SOD)活性高于模型组(P<0.05),丙二醛(Malondialdehyde,MDA)活性低于模型组(P<0.05),高剂量丁苯酞组与低剂量丁苯酞组对比差异都有统计学意义(P<0.05)。低剂量丁苯酞组与高剂量丁苯酞组治疗第21 d、第28 d的海马CA1区BCL2-Associated X(Bax)、B淋巴细胞瘤-2(B-cell lymphoma-2,bcl-2)蛋白相对表达水平高于模型组(P<0.05),高剂量丁苯酞组高于低剂量丁苯酞组(P<0.05)。结论:丁苯酞在颈动脉狭窄大鼠的应用能提高海马CA1区Bax、Bcl-2蛋白的表达,抑制神经元的凋亡,改善氧化应激状态,从而提高大鼠的认知功能。 |
英文摘要: |
ABSTRACT Objective: To explore and study the effect of butylphthalide on cognitive function and neuronal apoptosis in hippocampal CA1 area of rats with carotid artery stenosis and related mechanisms. Methods: Rats with carotid artery stenosis (n=42) were randomly divided into three groups-model group, low-dose butylphthalide(20 mg/kg) group and high-dose butylphthalide (40 mg/kg) group, each with 14 caes in each groups The low-dose butylphthalide group and the high-dose butylphthalide group were given 20 mg/kg and 40 mg/kg butylphthalide by gavage every day, and the control group were given the same dose of normal saline by gavage for 21 days. Results: The BBT scores of the low-dose butylphthalide group and the high-dose butylphthalide group were lower than those of the model group on the 7th, 14th, 21st days(P<0.05), and the high-dose butylphthalide group were lower than the low-dose butylphthalide group (P<0.05). The apoptosis index of hippocampal CA1 neurons in the low-dose butylphthalide group and the high-dose butylphthalide group were lower than that of the model group on the 21st and 28th day, and the high-dose butylphthalide group were lower than that of the low-dose butylphthalide group(P<0.05). The activity of superoxide dismutase (SOD) in the brain tissue of the low-dose butylphthalide group and the high-dose butylphthalide group were higher than that of the model group on the 21st and 28th day(P<0.05). Malondialdehyde (Malondialdehyde, The MDA activity were lower than that of the model group (P<0.05), and the difference compared between the high-dose butylphthalide group and the low-dose butylphthalide group were statistically significant (P<0.05). Treatment of BCL2-Associated X(Bax) and B-cell lymphoma-2(bcl-2) proteins in the hippocampal CA1 area on the 21st and 28th day of the low-dose butylphthalide group and the high-dose butylphthalide group The relative expression level were higher than the model group(P<0.05), and the high-dose butylphthalide group were higher than the low-dose butylphthalide group(P<0.05). Conclusion: The application of butylphthalide in rats with carotid artery stenosis can increase the expression of Bax and Bcl-2 protein in hippocampal CA1 area, inhibit neuronal apoptosis, improve oxidative stress, and improve the cognitive function of rats. |
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