仙茅苷对阿尔茨海默病大鼠行为学及海马神经元凋亡的影响
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摘要
目的探讨仙茅苷对阿尔茨海默病大鼠行为学及海马神经元凋亡的影响。方法将60只老年健康雄性SD大鼠腹腔注射D-半乳糖60 mg·kg~(-1),qd(连续6周)联合海马注射β-样淀粉蛋白25-35(Aβ25-35) 4 mmol·L~(-1),qd(第7周),构建阿尔茨海默病大鼠模型,并随机分为4组:低、中、高剂量实验组(建模期间予以灌胃仙茅苷24,48,72 mg·kg-1,qd),模型组(建模期间予以灌胃等量0. 9%Na Cl);另选15只老年健康雄性SD大鼠灌胃等量0. 9%Na Cl作为对照组。用Morris水迷宫实验检测各组大鼠学习记忆功能,用苏木精-伊红(HE)染色及细胞凋亡原位检测(TUNEL)法分别观察海马区神经元凋亡情况。结果对照组、模型组及低、中、高剂量实验组大鼠穿台次数分别为(15. 12±1. 78),(5. 03±1. 17),(7. 45±1. 36),(9. 79±1. 21)和(12. 33±1. 09)次,模型组分别与低、中、高剂量实验组比较,差异均有统计学意义(均P <0. 05);海马神经元凋亡比例分别(8. 42±2. 13)%,(69. 78±9. 97)%,(38. 14±8. 62)%,(24. 77±5. 43)%和(10. 02±1. 46)%,模型组分别与低、中、高剂量实验组比较,差异均有统计学意义(均P <0. 01)。结论仙茅苷可缓解海马神经元损伤,抑制海马神经元凋亡。
Objective To explore the effect of curculigoside on the behavior and hippocampal neuronal apoptosis of Alzheimer 's rats.Methods Sixty healthy old male SD rats were given intraperitoneal injection of 60 mg ·kg~(-1) of D-galactose once daily for 6 weeks and hippocampal injection of 4 mmol ·L~(-1) of β-like starch protein 25-35( Aβ25-35) on week 7 to induce Alzheimer's disease. Moreover,the rats were divided randomly into 4 groups: Experimental-L/-M/-H group( oral administration of 24,48,72 mg·kg~(-1) of curculigoside during modeling),model group( oral administration of equal amount of 0. 9%Na Cl during the modeling). A total of 15 healthy old male SD rats were set as control group and given oral administration of equal amount of0. 9% NaCl. The learning,memory function of rats in each group were evaluated by Morris water maze,the neuronal apoptosis in hippocampus were measured by hematoxylin eosin( HE) staining and Td T-mediated dUTP nick end labeling( TUNEL) method. Results The crossing platform number of rats in control group,model group and experimental-L/-M/-H groups were( 15. 12 ± 1. 78) times,( 5. 03 ± 1. 17) times,( 7. 45 ± 1. 36) times,( 9. 79 ± 1. 21) times and( 12. 33 ± 1. 09) times,respectively,and there were statistically significant differences between the model group and the experimental-L/-M/-H group( all P < 0. 05). The apoptosis ratio of hippocampus neurons were( 8. 42 ± 2. 13) %,( 69. 78 ± 9. 97) %,( 38. 14 ± 8. 62) %,( 24. 77 ± 5. 43) % and( 10. 02 ± 1. 46) %,respectively. There were statistically significant differences between the model group and the experimental-L/-M/-H group( all P < 0. 01). Conclusion Curculigoside can alleviate the damage of hippocampal neurons and inhibit the apoptosis of hippocampal neurons.
Objective To explore the effect of curculigoside on the behavior and hippocampal neuronal apoptosis of Alzheimer 's rats.Methods Sixty healthy old male SD rats were given intraperitoneal injection of 60 mg ·kg~(-1) of D-galactose once daily for 6 weeks and hippocampal injection of 4 mmol ·L~(-1) of β-like starch protein 25-35( Aβ25-35) on week 7 to induce Alzheimer's disease. Moreover,the rats were divided randomly into 4 groups: Experimental-L/-M/-H group( oral administration of 24,48,72 mg·kg~(-1) of curculigoside during modeling),model group( oral administration of equal amount of 0. 9%Na Cl during the modeling). A total of 15 healthy old male SD rats were set as control group and given oral administration of equal amount of0. 9% NaCl. The learning,memory function of rats in each group were evaluated by Morris water maze,the neuronal apoptosis in hippocampus were measured by hematoxylin eosin( HE) staining and Td T-mediated dUTP nick end labeling( TUNEL) method. Results The crossing platform number of rats in control group,model group and experimental-L/-M/-H groups were( 15. 12 ± 1. 78) times,( 5. 03 ± 1. 17) times,( 7. 45 ± 1. 36) times,( 9. 79 ± 1. 21) times and( 12. 33 ± 1. 09) times,respectively,and there were statistically significant differences between the model group and the experimental-L/-M/-H group( all P < 0. 05). The apoptosis ratio of hippocampus neurons were( 8. 42 ± 2. 13) %,( 69. 78 ± 9. 97) %,( 38. 14 ± 8. 62) %,( 24. 77 ± 5. 43) % and( 10. 02 ± 1. 46) %,respectively. There were statistically significant differences between the model group and the experimental-L/-M/-H group( all P < 0. 01). Conclusion Curculigoside can alleviate the damage of hippocampal neurons and inhibit the apoptosis of hippocampal neurons.
引文
[1]CUMMINGS J,LEE G,MORTSDORF T,et al.Alzheimer’s disease drug development pipeline:2017[J].Alzheimers Dement,2017,3(3):367-384.
[2]范鹏涛,张龙梅,闵恒,等.仙茅苷对血管性痴呆模型大鼠海马区Caspase-3、PARP-1和雌激素受体表达的作用[J].神经解剖学杂志,2017,33(4):453-458.
[3]赵璐,张巧艳,王泽剑,等.仙茅苷通过抗氧化作用改善APP/PS1小鼠的记忆和骨丢失[C]//药学学报药学前沿论坛暨2015年中国药学会中药与天然药物专业委员会会议.2015.
[4]刘娜,王金华,王华龙,等.红景天对阿尔茨海默病大鼠认知功能的治疗作用[J].河北医科大学学报,2017,38(2):133-137.
[5]彭璇,吴刚,吴昊,等.Morris水迷宫训练对阿尔茨海默病大鼠模型学习记忆能力及海马组织肿瘤坏死因子-α、超氧化物歧化酶、丙二醛水平的影响[J].中国老年学杂志,2017,37(8):1833-1835.
[6]王晗.淫羊藿苷对阿尔茨海默病模型小鼠的病理学影响及相关机制探讨[D].广州:广东药科大学,2016.
[7]李蓓华.脑缺血大鼠血清生长因子的动态变化及重组人生长激素对血管性痴呆模型大鼠作用的研究[D].泸州:西南医科大学,2017.
[8]曹梦园,赵月鸣,张晶,等.人参皂苷Rb1对Aβ25-35诱导痴呆大鼠海马神经元凋亡的影响[J].中国现代医学杂志,2015,25(35):33-36.
[2]范鹏涛,张龙梅,闵恒,等.仙茅苷对血管性痴呆模型大鼠海马区Caspase-3、PARP-1和雌激素受体表达的作用[J].神经解剖学杂志,2017,33(4):453-458.
[3]赵璐,张巧艳,王泽剑,等.仙茅苷通过抗氧化作用改善APP/PS1小鼠的记忆和骨丢失[C]//药学学报药学前沿论坛暨2015年中国药学会中药与天然药物专业委员会会议.2015.
[4]刘娜,王金华,王华龙,等.红景天对阿尔茨海默病大鼠认知功能的治疗作用[J].河北医科大学学报,2017,38(2):133-137.
[5]彭璇,吴刚,吴昊,等.Morris水迷宫训练对阿尔茨海默病大鼠模型学习记忆能力及海马组织肿瘤坏死因子-α、超氧化物歧化酶、丙二醛水平的影响[J].中国老年学杂志,2017,37(8):1833-1835.
[6]王晗.淫羊藿苷对阿尔茨海默病模型小鼠的病理学影响及相关机制探讨[D].广州:广东药科大学,2016.
[7]李蓓华.脑缺血大鼠血清生长因子的动态变化及重组人生长激素对血管性痴呆模型大鼠作用的研究[D].泸州:西南医科大学,2017.
[8]曹梦园,赵月鸣,张晶,等.人参皂苷Rb1对Aβ25-35诱导痴呆大鼠海马神经元凋亡的影响[J].中国现代医学杂志,2015,25(35):33-36.