银杏叶总黄酮对大鼠血瘀合并脑缺血再灌注模型氧化应激的干预作用
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摘要
目的:探讨银杏叶总黄酮对大鼠血瘀合并脑缺血再灌注模型氧化应激反应的影响。方法:采用连续肌肉注射地塞米松制造血瘀模型,银杏叶总黄酮混悬液大、小剂量(300 mg·kg~(-1)、150 mg·kg~(-1))、阳性药华佗再造丸(2.67 g·kg~(-1))连续给药10 d,于第11天给药1 h后,分离双侧颈总动脉夹闭30 min复制脑缺血模型,再灌注1 h后取血,肝素抗凝测全血黏度,断头冰盘剥脑,矢状切取一半置于体积分数10%福尔马林固定,用于HE染色;另一半脑组织称质量加适量冰生理盐水制备体积分数10%脑组织匀浆,测定丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide orgotein dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)水平。结果:血瘀合并脑缺血再灌注模型复制成功。与血瘀缺血组相比,银杏叶总黄酮大剂量可显著降低大鼠全血黏度高、中、低切值(P<0.01),小剂量组高切值、中切值具有明显降低趋势(P<0.05),低切值降低幅度更为显著(P<0.01);银杏叶总黄酮大剂量组可显著降低MDA含量(P<0.01),小剂量组可明显降低大鼠脑组织中MDA含量(P<0.05);银杏叶总黄酮大剂量可显著升高SOD、GSH-Px活性(P<0.01),小剂量可显著升高SOD活性(P<0.01),明显升高GSH-Px活性(P<0.05);银杏叶总黄酮大剂量组可显著改善大鼠脑缺血损伤后脑组织病理改变,趋势明显。结论:银杏叶总黄酮可显著抑制大鼠缺血后脑组织氧化应激反应,改善大鼠血瘀合并脑缺血模型的脑缺血损伤。
Objective:To investigate the effects of total flavonoids from Ginkgo biloba leaves on oxidative stress in rats with cerebral ischemia-reperfusion injury.Methods:The continuous intramuscular injection of dexamethasone hematopoietic model,large and small doses of ginkgo biloba leaf flavonoid suspension(300 mg·kg~(-1),150 mg·kg~(-1)),and positive drug Huajing reconstituted pills(2.67 g·kg~(-1)) continuous administration for 10 days,1 hour after the 11 th day of administration,the bilateral common carotid artery was clamped for 30 minutes to replicate the cerebral ischemia model,and blood was taken 1 hour after reperfusion.Heparin anticoagulation measured whole blood viscosity.,decapitated ice disc stripping brain,sagittal cut half placed in a volume fraction of 10% formalin fixed for HE staining;the other half of the brain tissue weighing plus appropriate amount of ice physiological saline to prepare a volume fraction of 10% brain tissue homogenate,determination Malondialdehyde(MDA),superoxide orgotein dismutase(SOD),glutathione peroxidase(GSH-Px) levels.Results:The blood stasis combined with cerebral ischemia-reperfusion model was successfully replicated.Compared with the blood stasis group,the high dose of total flavonoids in Ginkgo biloba leaves can significantly reduce the high,medium and low cut values of whole blood viscosity in rats(P<0.01).The high cut and medium cut values of the low dose group have a significant decrease trend.(P<0.05),the decrease of low cut value was more significant(P<0.01);the high dose of total flavonoids in Ginkgo biloba leaves could significantly reduce MDA content(P<0.01),and the low dose group could significantly reduce MDA in rat brain tissue.The content of total flavonoids in Ginkgo biloba leaves could significantly increase the activity of SOD and GSH-Px(P<0.01).The low dose could significantly increase the activity of SOD(P<0.01) and significantly increase the activity of GSH-Px(P<0.05);Ginkgo biloba total flavonoids in the high-dose group can significantly improve the pathological changes of brain tissue after cerebral ischemic injury in rats,and the trend is obvious.Conclusion:Ginkgo biloba leaf flavonoids can significantly inhibit oxidative stress in rat brain after ischemia and improve cerebral ischemic injury in rats with blood stasis and cerebral ischemia.
Objective:To investigate the effects of total flavonoids from Ginkgo biloba leaves on oxidative stress in rats with cerebral ischemia-reperfusion injury.Methods:The continuous intramuscular injection of dexamethasone hematopoietic model,large and small doses of ginkgo biloba leaf flavonoid suspension(300 mg·kg~(-1),150 mg·kg~(-1)),and positive drug Huajing reconstituted pills(2.67 g·kg~(-1)) continuous administration for 10 days,1 hour after the 11 th day of administration,the bilateral common carotid artery was clamped for 30 minutes to replicate the cerebral ischemia model,and blood was taken 1 hour after reperfusion.Heparin anticoagulation measured whole blood viscosity.,decapitated ice disc stripping brain,sagittal cut half placed in a volume fraction of 10% formalin fixed for HE staining;the other half of the brain tissue weighing plus appropriate amount of ice physiological saline to prepare a volume fraction of 10% brain tissue homogenate,determination Malondialdehyde(MDA),superoxide orgotein dismutase(SOD),glutathione peroxidase(GSH-Px) levels.Results:The blood stasis combined with cerebral ischemia-reperfusion model was successfully replicated.Compared with the blood stasis group,the high dose of total flavonoids in Ginkgo biloba leaves can significantly reduce the high,medium and low cut values of whole blood viscosity in rats(P<0.01).The high cut and medium cut values of the low dose group have a significant decrease trend.(P<0.05),the decrease of low cut value was more significant(P<0.01);the high dose of total flavonoids in Ginkgo biloba leaves could significantly reduce MDA content(P<0.01),and the low dose group could significantly reduce MDA in rat brain tissue.The content of total flavonoids in Ginkgo biloba leaves could significantly increase the activity of SOD and GSH-Px(P<0.01).The low dose could significantly increase the activity of SOD(P<0.01) and significantly increase the activity of GSH-Px(P<0.05);Ginkgo biloba total flavonoids in the high-dose group can significantly improve the pathological changes of brain tissue after cerebral ischemic injury in rats,and the trend is obvious.Conclusion:Ginkgo biloba leaf flavonoids can significantly inhibit oxidative stress in rat brain after ischemia and improve cerebral ischemic injury in rats with blood stasis and cerebral ischemia.
引文
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[8]张永英.胡黄连苷Ⅱ对大鼠脑缺血损伤后MDA含量和SOD活性的影响[D].青岛:青岛大学,2013.
[9]陈鹏,丁志杰.熊果酸对大鼠局灶性脑缺血再灌注损伤的保护作用[J].中国实验方剂学杂志,2015,21(12):129-133.
[10]陈燕,崔苏扬,田伟千,等.电针对脑缺血-再灌注损伤大鼠脑组织SOD和IL-1β含量的影响[J].江苏医药,2011,37(4):393-395.
[2]李红军.银杏叶中黄酮类化合物的提取及其体外抗氧化活性研究[J].北方园艺,2013,37(5):156-159.
[3]苗明三,程再兴,宰炎冰,等.大鼠血瘀合并脑缺血模型的建立[J].中药新药与临床药理,2007,18(1):1-5.
[4]李显华,杜佳林,包玉龙,等.丹龙胶囊对脑缺血模型动物的保护作用[J].中国实验方剂学杂志,2011,17(22):219-220.
[5]张帆,张小磊,苗明三.毛冬青总黄酮对大鼠血瘀合并脑缺血模型的影响[J].中国实验方剂学杂志,2012,18(22):187-191.
[6]程晓,张小莉,白明,等.活血化瘀法、清热解毒法对脑缺血的防治特点及分析[J].中医学报,2012,27(5):615-619.
[7]白明,高小玲,苗明三.脑脉舒康胶囊对大鼠血瘀合并脑缺血模型能量代谢的影响[J].中国实验方剂学杂志,2012,18(11):209-211.
[8]张永英.胡黄连苷Ⅱ对大鼠脑缺血损伤后MDA含量和SOD活性的影响[D].青岛:青岛大学,2013.
[9]陈鹏,丁志杰.熊果酸对大鼠局灶性脑缺血再灌注损伤的保护作用[J].中国实验方剂学杂志,2015,21(12):129-133.
[10]陈燕,崔苏扬,田伟千,等.电针对脑缺血-再灌注损伤大鼠脑组织SOD和IL-1β含量的影响[J].江苏医药,2011,37(4):393-395.