阿托伐他汀对老年大鼠心肌H_2O_2、MDA及GSH-Px水平的影响分析
摘要
目的分析阿托伐他汀对老年大鼠心肌过氧化氢(H2O2)、血清丙二醛(MDA)及谷胱甘肽过氧化物酶(GSH-Px)水平的影响。方法选取30只3个月龄Wistar大鼠设定为青年对照组,不对其进行任何处理,只正常饲养;另选取90只10个月龄Wistar大鼠,将其饲养到20个月龄后随机分为高剂量组、低剂量组、老年对照组,每组30只。高剂量组给予大鼠10 mg/(kg·d)阿托伐他汀灌胃,低剂量组给予大鼠1 mg/(kg·d)阿托伐他汀灌胃,给予老年对照组大鼠等体积0.9%氯化钠溶液灌胃,比较四组大鼠的心肌H_2O_2、MDA及GSH-Px水平。结果高剂量组H_2O_2、MDA、GSH-Px水平分别为(4.7±1.4)nmol/g、(64.2±15.7)nmol/mg prot、(25.3±6.8)U/mg prot,低剂量组分别为(5.8±1.5)nmol/g、(77.3±14.0)nmol/mg prot、(20.6±5.7)U/mg prot,老年对照组分别为(7.0±2.0)nmol/g、(98.4±16.2)nmol/mg prot、(15.0±5.2)U/mg prot,青年对照组分别为(3.6±1.3)nmol/g、(50.8±11.0)nmol/mg prot、(30.5±8.6)U/mg prot;高剂量组、低剂量组、老年对照组大鼠的心肌H_2O_2、MDA水平均高于青年对照组, GSH-Px水平均低于青年对照组,差异有统计学意义(P<0.05);高剂量组和低剂量组大鼠的心肌H_2O_2、MDA水平均低于老年对照组, GSH-Px水平高于老年对照组,差异有统计学意义(P<0.05)。结论阿托伐他汀能够有效改善老年大鼠心肌H_2O_2、MDA及GSH-Px水平。
引文
[1]Lu J, Liu F, Liu D, et al. Amlodipine and atorvastatin improved hypertensive cardiac hypertrophy through regulation of receptor activator of nuclear factor kappa B ligand/receptor activator of nuclear factor kappa B/osteoprotegerin system in spontaneous hypertension rats. Experimental Biology&Medicine, 2016,241(11):1237-1249.
[2]韩磊,叶平,李鸣皋.阿托伐他汀对老年大鼠心肌过氧化氢、丙二醛及谷胱甘肽过氧化物酶水平的影响.解放军医药杂志,2014, 26(2):44-46.
[3]黄可欣,石博,叶保国,等.阿托伐他汀对心肌缺血再灌注损伤大鼠心肌酶和心肌细胞凋亡的影响及其心肌保护作用机制.吉林大学学报(医学版), 2013, 39(5):923-927,后插4.
[4]Liang J, Yin K, Cao X, et al. Attenuation of Low Ambient Temperature-Induced Myocardial Hypertrophy by Atorvastatin via Promoting Bcl-2 Expression. Cell Physiol Biochem, 2017,41(1):286-295.
[5]Chen L, Cai P, Cheng Z, et al. Pharmacological postconditioning with atorvastatin calcium attenuates myocardial ischemia/reperfusion injury in diabetic rats by phosphorylating GSK3β. Exp Ther Med,2017, 14(1):25-34.
[6]Yang C, Zhao D, Liu G, et al. Atorvastatin Attenuates Metabolic Remodeling in Ischemic Myocardium through the Downregulation of UCP2 Expression. Int J Med Sci, 2018, 15(5):517-527.
[7]Chen Y, Chang Y, Zhang N, et al. Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway. Cell Physiol Biochem, 2018,46(3):1009-1018.
[8]Gao X, Yang J, Zhang X, et al. A case report of apical aneurysms and myocardial perfusion deficit with myocardial necrosis due to hypertrophic cardiomyopathy. Medicine(Baltimore), 2018,97(21):e10829.
[2]韩磊,叶平,李鸣皋.阿托伐他汀对老年大鼠心肌过氧化氢、丙二醛及谷胱甘肽过氧化物酶水平的影响.解放军医药杂志,2014, 26(2):44-46.
[3]黄可欣,石博,叶保国,等.阿托伐他汀对心肌缺血再灌注损伤大鼠心肌酶和心肌细胞凋亡的影响及其心肌保护作用机制.吉林大学学报(医学版), 2013, 39(5):923-927,后插4.
[4]Liang J, Yin K, Cao X, et al. Attenuation of Low Ambient Temperature-Induced Myocardial Hypertrophy by Atorvastatin via Promoting Bcl-2 Expression. Cell Physiol Biochem, 2017,41(1):286-295.
[5]Chen L, Cai P, Cheng Z, et al. Pharmacological postconditioning with atorvastatin calcium attenuates myocardial ischemia/reperfusion injury in diabetic rats by phosphorylating GSK3β. Exp Ther Med,2017, 14(1):25-34.
[6]Yang C, Zhao D, Liu G, et al. Atorvastatin Attenuates Metabolic Remodeling in Ischemic Myocardium through the Downregulation of UCP2 Expression. Int J Med Sci, 2018, 15(5):517-527.
[7]Chen Y, Chang Y, Zhang N, et al. Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway. Cell Physiol Biochem, 2018,46(3):1009-1018.
[8]Gao X, Yang J, Zhang X, et al. A case report of apical aneurysms and myocardial perfusion deficit with myocardial necrosis due to hypertrophic cardiomyopathy. Medicine(Baltimore), 2018,97(21):e10829.