尼莫地平不同时间给药对血管性痴呆小鼠氧自由基代谢的影响
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摘要
目的:不同时间给予尼莫地平治疗血管性痴呆(VD)小鼠,观察小鼠脑组织氧自由基水平的变化。方法:将健康昆明小鼠随机分为假手术组、模型组、尼莫地平造模后即刻给药组、尼莫地平造模3 d后给药组,后3组小鼠反复结扎双侧颈动脉同时加尾部放血制作VD模型,两个尼莫地平给药组分别于造模后即刻、造模后3 d灌服尼莫地平,模型组及假手术组均每日3次灌服注射用生理盐水,治疗10 d后检测4组小鼠脑组织丙二醛(MDA)含量及SOD活性的变化。结果:模型组小鼠脑组织中MDA含量比假手术组显著增高(P<0.05),尼莫地平两个治疗组小鼠脑组织中MDA含量均明显低于模型组(P<0.05),且尼莫地平造模后即刻给药组MDA含量比尼莫地平造模3 d后给药组更低(P<0.05);模型组小鼠中SOD活性比假手术组显著降低;尼莫地平两个治疗组脑组织中SOD活性较模型组显著增高,且尼莫地平造模后即刻给药组比尼莫地平造模3 d后给药组更高(P<0.05)。结论:尼莫地平能降低痴呆小鼠体内MDA含量,提高SOD活性,即刻给药组的疗效优于3 d后给药组,所以VD一旦确诊应尽快给予尼莫地平干预,以预防病情的进一步发展。
Objective:To observe the changes of oxygen free radical metabolism in brain tissue of vascular dementia mice caused by nimodipine administered at different time points. Methods:Forty healthy Kunming mice were randomly divided into 4 groups:sham-operation group( group S),model group( group M),and nimodipine treated groups( group N1,received nimodipine on day 0,and group N2 received nimodipine on day 3). The models of vascular dementia mice were induced by repeated ligation of bilateral common carotid arteries and tail bloodletting. The mice in groups N1 and N2 were respectively given nimodipine on 0,and 3rd days after the models were established,and mice in groups S and M were given normal saline instead. Ten days after treatment,the contents of oxygen free radical metabolism in mice brain tissue were measured. Result:The content of oxygen free radical malondialdehyde( MDA) was significantly higher in group M than in group S( P < 0. 05),lower in two nimodipine treatment groups than in group M( P < 0. 05),and significantly lower in group N1 than in group N2( P < 0. 05). The activity of oxygen free radical superoxide dismutase( SOD) was significantly lower in group M than in group S( P < 0. 05),higher in two nimodipine treatment groups than in group M( P < 0. 05) and higher in group N1 than in group N2( P < 0. 05). Conclusion:Nimodipine can decrease the content of MDA in mice with dementia,and improve the activity of SOD,and the curative effect of the immediate treatment group was better than that of the 3-days later treatment group. Therefore,once vascular dementia is diagnosed patient should be treated immediately,so as to obtain better therapeutic effect.
Objective:To observe the changes of oxygen free radical metabolism in brain tissue of vascular dementia mice caused by nimodipine administered at different time points. Methods:Forty healthy Kunming mice were randomly divided into 4 groups:sham-operation group( group S),model group( group M),and nimodipine treated groups( group N1,received nimodipine on day 0,and group N2 received nimodipine on day 3). The models of vascular dementia mice were induced by repeated ligation of bilateral common carotid arteries and tail bloodletting. The mice in groups N1 and N2 were respectively given nimodipine on 0,and 3rd days after the models were established,and mice in groups S and M were given normal saline instead. Ten days after treatment,the contents of oxygen free radical metabolism in mice brain tissue were measured. Result:The content of oxygen free radical malondialdehyde( MDA) was significantly higher in group M than in group S( P < 0. 05),lower in two nimodipine treatment groups than in group M( P < 0. 05),and significantly lower in group N1 than in group N2( P < 0. 05). The activity of oxygen free radical superoxide dismutase( SOD) was significantly lower in group M than in group S( P < 0. 05),higher in two nimodipine treatment groups than in group M( P < 0. 05) and higher in group N1 than in group N2( P < 0. 05). Conclusion:Nimodipine can decrease the content of MDA in mice with dementia,and improve the activity of SOD,and the curative effect of the immediate treatment group was better than that of the 3-days later treatment group. Therefore,once vascular dementia is diagnosed patient should be treated immediately,so as to obtain better therapeutic effect.
引文
[1]张立,邢艳丽,熊伟南.血管性痴呆治疗的研究进展[J].医学综述,2015(8):1414-1417.
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[4]孙丽芳,张丽欣,邢利和.补阳还五方不同时间给药对血管性痴呆小鼠行为学的影响[J].河北中医药学报,2016(1):5-7.
[5]袁野,杨俊卿,周岐新.脑缺血再灌注致小鼠神经元退行性变进程中自由基水平和SOD-1表达的变化[J].第三军医大学学报,2011(12):1211-1215.
[6]陈贺华,刘勇,沈晓明.依达拉奉对急性脑梗死患者血清丙二醛和超氧化物歧化酶含量及神经功能的影响[J].中国现代药物应用,2014(13):159-161.
[7]罗招凡,劳伟思,梁伟南.血清同型半胱氨酸和SOD水平与急性脑梗死的相关性研究[J].中国卫生检验杂志,2011(10):2463-2464.
[8]陈乾兵.尼莫地平对脑卒中后血管性认知障碍的临床效果[J].吉林医学,2015(7):1359-1360.
[9]李孟,张晓华.尼莫地平的药理作用及临床应用[J].中国实用医药,2013(13):201-202.
[10]郭付清.超早期应用尼莫地平对脑缺血大鼠一氧化氮和自由基的影响[J].山东医药,2006(17):79-80.
[11]张根平.尼莫地平治疗血管性痴呆92例临床报道[J].中国医药指南,2015(16):112-113.
[12]王慧霞.脑缺血半暗带及其干预的研究进展[J].世界最新医学信息文摘,2014(14):52-53.
[13]汪利,李国忠.缺血性卒中与脑侧支循环[J].中国医师进修杂志,2014(31):70-72.
[2]周晓秋.尼莫地平在血管性痴呆治疗应用[J].中国老年保健医学,2013(6):63-64.
[3]张艳,李倩倩,霍薇.血管性痴呆动物模型的研究现状[J].中国神经免疫学和神经病学杂志,2015(1):67-70.
[4]孙丽芳,张丽欣,邢利和.补阳还五方不同时间给药对血管性痴呆小鼠行为学的影响[J].河北中医药学报,2016(1):5-7.
[5]袁野,杨俊卿,周岐新.脑缺血再灌注致小鼠神经元退行性变进程中自由基水平和SOD-1表达的变化[J].第三军医大学学报,2011(12):1211-1215.
[6]陈贺华,刘勇,沈晓明.依达拉奉对急性脑梗死患者血清丙二醛和超氧化物歧化酶含量及神经功能的影响[J].中国现代药物应用,2014(13):159-161.
[7]罗招凡,劳伟思,梁伟南.血清同型半胱氨酸和SOD水平与急性脑梗死的相关性研究[J].中国卫生检验杂志,2011(10):2463-2464.
[8]陈乾兵.尼莫地平对脑卒中后血管性认知障碍的临床效果[J].吉林医学,2015(7):1359-1360.
[9]李孟,张晓华.尼莫地平的药理作用及临床应用[J].中国实用医药,2013(13):201-202.
[10]郭付清.超早期应用尼莫地平对脑缺血大鼠一氧化氮和自由基的影响[J].山东医药,2006(17):79-80.
[11]张根平.尼莫地平治疗血管性痴呆92例临床报道[J].中国医药指南,2015(16):112-113.
[12]王慧霞.脑缺血半暗带及其干预的研究进展[J].世界最新医学信息文摘,2014(14):52-53.
[13]汪利,李国忠.缺血性卒中与脑侧支循环[J].中国医师进修杂志,2014(31):70-72.