他汀类药物对心肌缺血再灌注损伤心肌细胞凋亡作用机制的研究进展

被引：6

作者：

苏强

李浪

机构：

[1] 广西医科大学第一附属医院心内科广西心血管病研究所

来源：

心血管病学进展 | 2010年 / 31卷 / 01期

关键词：

他汀类药物; 心肌细胞; 凋亡; 缺血再灌注损伤;

D O I：

暂无

中图分类号：

R965.1 [药物筛选和实验模型];

学科分类号：

100706 [药理学];

摘要：

近年研究表明,细胞凋亡在心肌缺血再灌注损伤(MIRI)中占有重要地位,细胞凋亡与MIRI之间有着密切关系。实验证实他汀类药物具有除调脂以外的心肌保护效应。现主要从他汀类药物的抗氧化作用和激活磷脂酰肌醇-3-激酶丝氨酸-苏氨酸激酶/一氧化氮合酶(PI3K/Akt/eNOS)信号通路两个方面阐述在心肌缺血再灌注过程中他汀类药物抑制心肌细胞凋亡的主要机制。

引用

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页码：134 / 137

页数：4

相关论文

共 14 条

[1]

Effect of Acute and Chronic Simvastatin Treatment on Post-Ischemic Contractile Dysfunction in Isolated Rat Heart [J].

Szarszoi, O. ;

Maly, J. ;

Ostadal, P. ;

Netuka, I. ;

Besik, J. ;

Kolar, F. ;

Ostadal, B. .

PHYSIOLOGICAL RESEARCH, 2008, 57 (05) :793-796

[2]

ASK1 is activated by arsenic trioxide in leukemic cells through accumulation of reactive oxygen species and may play a negative role in induction of apoptosis [J].

Yan, Weihua ;

Arai, Ayako ;

Aoki, Mae ;

Ichijo, Hidenori ;

Miura, Osamu .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2007, 355 (04) :1038-1044

[3]

The protective effect of HMG-CoA reductase inhibitors against monocrotaline-induced pulmonary hypertension in the rat might not be a class effect: comparison of pravastatin and atorvastatin [J].

Rakotoniaina, Zo ;

Guerard, Pascal ;

Lirussi, Frederic ;

Goirand, Francoise ;

Rochette, Luc ;

Dumas, Monique ;

Bardou, Marc .

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, 2006, 374 (03) :195-206

[4]

Clinical implications of apoptosis in ischemic myocardium [J].

Scarabelli, TM ;

Knight, R ;

Stephanou, A ;

Townsend, P ;

Chen-Scarabelli, C ;

Lawrence, K ;

Gottlieb, R ;

Latchman, D ;

Narula, J .

CURRENT PROBLEMS IN CARDIOLOGY, 2006, 31 (03) :181-264

[5]

Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK [J].

Moolman, JA ;

Hartley, S ;

Van Wyk, J ;

Marais, E ;

Lochner, A .

CARDIOVASCULAR DRUGS AND THERAPY, 2006, 20 (01) :13-25

[6]

Human endothelial nitric oxide synthase gene delivery protects against cardiac remodeling and reduces oxidative stress after myocardial infarction [J].

Smith, RS ;

Agata, J ;

Xia, CF ;

Chao, L ;

Chao, J .

LIFE SCIENCES, 2005, 76 (21) :2457-2471

[7]

Simvastatin acutely reduces myocardial reperfusion injury in vivo by activating the phosphatidylinositide 3-kinase/Akt pathway [J].

Wolfrum, S ;

Dendorfer, A ;

Schutt, M ;

Weidtmann, B ;

Heep, A ;

Tempel, K ;

Klein, HH ;

Dominiak, P ;

Richardt, G .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2004, 44 (03) :348-355

[8]

Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion [J].

Zhang, HF ;

Fan, Q ;

Qian, XX ;

Lopez, BL ;

Christopher, TA ;

Ma, XL ;

Gao, F .

APOPTOSIS, 2004, 9 (06) :777-783

[9]

Simvastatin preserves cardiac function in genetically determined cardiomyopathy [J].

Abraham, SS ;

Osorio, JC ;

Homma, S ;

Wang, J ;

Thaker, HM ;

Liao, JK ;

Mital, S .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2004, 43 (03) :454-461

[10]

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors prevent the development of cardiac hypertrophy and heart failure in rats [J].

Hasegawa, H ;

Yamamoto, R ;

Takano, H ;

Mizukami, M ;

Asakawa, M ;

Nagai, T ;

Komuro, I .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2003, 35 (08) :953-960