黄芪对缺血再灌注诱导心肌损伤的保护作用
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摘要
目的:探讨黄芪对缺血再灌注诱导的心肌损伤的保护作用。方法:收集60只正常大鼠建立缺血再灌注损伤模型,随机分为对照组、缺血再灌注模型组、实验组,各20只。实验组在大鼠进行再灌注损伤造模时,给予5 mL黄芪浓缩液,缺血再灌注模型组给予等体积的生理盐水进行干预,对照组不做任何处理。造模成功24 h后迅速断头取心,采用MTT比色法检测细胞增殖能力;采用TUNEL(TdT-mediated dUTP Nick-End Labeling)法检测细胞凋亡率,进一步验证其保护作用;采用蛋白免疫印迹(Western blot)法检测蛋白激酶B(protein kinase B,PKB)、超氧化物歧化酶(superoxide orgotein dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH)水平。结果:与对照组比较,缺血再灌注模型组和实验组细胞增殖能力明显降低,细胞凋亡率能力明显增加,PKB、SOD、GSH水平明显升高,差异具有统计学意义(P<0.05);与缺血再灌注模型组比较,实验组细胞增殖能力明显增加,细胞凋亡率明显减少,PKB、SOD、GSH水平存在明显变化,差异具有统计学意义(P<0.05)。结论:黄芪可减轻心肌细胞的缺血再灌注损伤,通过抗氧化和抗凋亡来实现保护作用。
Objective:To investigate the protective effect of Astragalus membranaceus on myocardial injury induced by ischemia reperfusion.Methods:A total of 60 normal rats were randomly divided into control group,ischemia/reperfusion model group and experimental group,20 rats each.In the experimental group,5 mL of Astragalus membranaceus was given during reperfusion injury,and an isotonic/reperfusion model group was given an equal volume of physiological saline for intervention.The control group did not do any treatment.After 24 hours of successful modeling,the mice were quickly decapitated and the cell proliferation ability was detected by MTT colorimetry.The TUNEL(TdT-mediated dUTP Nick-End Labeling) method was used to detect the apoptosis rate to further verify its protective effect.Western blot analysis was used to detect the expression of protein kinase B(PKB),superoxide orgotein dismutase(SOD) and glutathione peroxidase(GSH).Results:Compared with that of the control group,the cell proliferation ability of the ischemia/reperfusion model group and the experimental group was significantly decreased,the apoptosis rate ability was significantly increased,and the expressions of PKB,SOD,GSH levels and other proteins were significantly increased,and the difference was statistically significant(P<0.05);Compared with that of the ischemia/reperfusion model group,the cell proliferation ability of the experimental group was significantly increased,the apoptosis rate ability was significantly reduced,and the expressions of PKB,SOD,GSH levels and other proteins were significantly different(P<0.05).Conclusion:Astragalus membranaceus can alleviate the ischemia-reperfusion injury of cardiomyocytes,and achieve protection through anti-oxidation and anti-apoptosis.
Objective:To investigate the protective effect of Astragalus membranaceus on myocardial injury induced by ischemia reperfusion.Methods:A total of 60 normal rats were randomly divided into control group,ischemia/reperfusion model group and experimental group,20 rats each.In the experimental group,5 mL of Astragalus membranaceus was given during reperfusion injury,and an isotonic/reperfusion model group was given an equal volume of physiological saline for intervention.The control group did not do any treatment.After 24 hours of successful modeling,the mice were quickly decapitated and the cell proliferation ability was detected by MTT colorimetry.The TUNEL(TdT-mediated dUTP Nick-End Labeling) method was used to detect the apoptosis rate to further verify its protective effect.Western blot analysis was used to detect the expression of protein kinase B(PKB),superoxide orgotein dismutase(SOD) and glutathione peroxidase(GSH).Results:Compared with that of the control group,the cell proliferation ability of the ischemia/reperfusion model group and the experimental group was significantly decreased,the apoptosis rate ability was significantly increased,and the expressions of PKB,SOD,GSH levels and other proteins were significantly increased,and the difference was statistically significant(P<0.05);Compared with that of the ischemia/reperfusion model group,the cell proliferation ability of the experimental group was significantly increased,the apoptosis rate ability was significantly reduced,and the expressions of PKB,SOD,GSH levels and other proteins were significantly different(P<0.05).Conclusion:Astragalus membranaceus can alleviate the ischemia-reperfusion injury of cardiomyocytes,and achieve protection through anti-oxidation and anti-apoptosis.
引文
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[8]王敏杰,金蓉,李慧芳.蒙古黄芪总黄酮对大鼠心肌缺血再灌注损伤的保护作用[J].中南药学,2015,13(2):147-150.
[9]LIN J,WANG H,LI J,et al.κ-Opioid receptor stimulation modulates TLR4/NF-κB signaling in the rat heart subjected to ischemia-reperfusion[J].Cytokine,2013,61(3):842-848.
[10]曹明明,高彦宇,马育轩,等.黄芪化学成分及对心肌缺血再灌注损伤保护作用的研究进展[J].中医药信息,2015,32(3):120-123.
[11]WU Y,LIU Y,HUANG H,et al.Dexmedetomidine inhibits inflammatory reaction in lung tissues of septic rats by suppressing TLR4/NF-κB pathway[J].Mediators Inflamm,2013,56(54):1-9.
[12]邢晓雪,李玲燕,高慧,等.黄芪甲苷对心脏缺血再灌注损伤的保护作用研究现状[J].中国临床药理学杂志,2016,32(18):1726-1728.
[13]李铁成,马宝丰,李德生,等.黄芪甲苷对大鼠肝缺血/再灌注损伤的保护作用[J].天津中医药,2014,31(10):621-623.
[14]贺永贵,李王芳,伊红丽,等.黄芪甲苷抑制GSK-3β活性介导大鼠心肌缺血/再灌注损伤作用的线粒体机制研究[J].中国药理学通报,2014,30(3):402-406.
[15]孙丽,王岭,李艳,等.黄芪甲苷对大鼠脑缺血再灌注损伤的保护作用和机制研究[J].中国临床神经科学,2014,22(1):43-49.
[2]李铁成,张静峰,马宝丰,等.黄芪多糖对心肌缺血再灌注损伤的保护作用[J].天津中医药,2014,31(8):490-492.
[3]GUO J,WANG S B,YUAN T Y,et al.Coptisine protects rat heart against myocardial ischemia /reperfusion injury by suppressing myocardial apoptosis and inflammation[J].Atherosclerosis,2013,23(2):384-391.
[4]屈玉春,王大伟,严夏,等.黄芪甲苷降低缺血再灌注诱导的大鼠心肌损伤[J].中国老年学杂志,2014,34(12):3204-3205.
[5]马小亮,王桂敏.黄芪甲苷灌胃预处理对大鼠心肌缺血再灌注损伤的保护作用[J].中国老年学杂志,2015,35(17):4795-4796.
[6]张静,马翠丽,王志国.黄芪甲苷对大鼠心肌局部缺血再灌注损伤的改善作用及其对PI3K/PKB/mTOR信号通路的影响[J].吉林大学学报(医学版),2014,40(5):991-994.
[7]郭保伟,付刚,刘艳梅,等.黄芪对大鼠肾脏缺血再灌注损伤的保护作用及其对细胞凋亡影响的研究[J].中国实用医药,2014,9(17):244-246.
[8]王敏杰,金蓉,李慧芳.蒙古黄芪总黄酮对大鼠心肌缺血再灌注损伤的保护作用[J].中南药学,2015,13(2):147-150.
[9]LIN J,WANG H,LI J,et al.κ-Opioid receptor stimulation modulates TLR4/NF-κB signaling in the rat heart subjected to ischemia-reperfusion[J].Cytokine,2013,61(3):842-848.
[10]曹明明,高彦宇,马育轩,等.黄芪化学成分及对心肌缺血再灌注损伤保护作用的研究进展[J].中医药信息,2015,32(3):120-123.
[11]WU Y,LIU Y,HUANG H,et al.Dexmedetomidine inhibits inflammatory reaction in lung tissues of septic rats by suppressing TLR4/NF-κB pathway[J].Mediators Inflamm,2013,56(54):1-9.
[12]邢晓雪,李玲燕,高慧,等.黄芪甲苷对心脏缺血再灌注损伤的保护作用研究现状[J].中国临床药理学杂志,2016,32(18):1726-1728.
[13]李铁成,马宝丰,李德生,等.黄芪甲苷对大鼠肝缺血/再灌注损伤的保护作用[J].天津中医药,2014,31(10):621-623.
[14]贺永贵,李王芳,伊红丽,等.黄芪甲苷抑制GSK-3β活性介导大鼠心肌缺血/再灌注损伤作用的线粒体机制研究[J].中国药理学通报,2014,30(3):402-406.
[15]孙丽,王岭,李艳,等.黄芪甲苷对大鼠脑缺血再灌注损伤的保护作用和机制研究[J].中国临床神经科学,2014,22(1):43-49.
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