| 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].,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 |
| 投稿时间：2021-11-05 修订日期：2021-11-30 |
| 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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