Department of Pharmacology, School of Pharmacy, Suez Canal University, Ismailia, Egypt.
Eur Rev Med Pharmacol Sci. 2010 Jun;14(6):499-506.
Pro- and anti-inflammatory cytokines play a major role in the development of acute myocardial infarction (AMI). This paper tests the hypothesis that atorvastatin may attenuate the severity of myocardial ischemic injury by restoring the balance between pro-inflammatory and anti-inflammatory mediators.
Sixty adult male albino rats were used. Experimental AMI was induced by subcutaneous injection of isoprenaline. Atorvastatin was given for five days, then, it was combined with isoprenaline in the last two days of treatment protocol. Rats without any treatment were used as controls. Rats were subjected to ECG tracing, assessment of Creatine phosphokinase (CPK) and CPK-MB, measurements of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10), and plasminogen activator inhibitor-1 (PAI-1).
Induction of AMI by isoprenaline resulted in a significant elevation of ST segment, elevation of CPK and CPK-MB. CRP, TNF-alpha and plasma PAI-1 were significantly elevated in the AMI rats compared to the control groups. On the other hand, the level of the anti-inflammatory cytokine IL-10 was significantly reduced. Treatment with atorvastatin prior to induction of AMI was associated with a significant reduction of serum CRP, TNF-alpha, plasma PAI-1 and an increase of serum IL-10.
This study suggests the usefulness of atorvastatin as an attenuating agent against AMI. Atorvastatin restores the balance between the pro-inflammatory and the anti-inflammatory mediators and modulates the fibrinolysis by reducing the levels of PAI-1.
促炎和抗炎细胞因子在急性心肌梗死（AMI）的发展中起主要作用。本文通过测试阿托伐他汀通过恢复促炎和抗炎介质之间的平衡来减轻心肌缺血性损伤严重程度的假说。
使用 60 只成年雄性白化大鼠。通过皮下注射异丙肾上腺素诱导实验性 AMI。阿托伐他汀治疗 5 天，然后在治疗方案的最后两天与异丙肾上腺素联合使用。未接受任何治疗的大鼠作为对照。对大鼠进行心电图描记、肌酸磷酸激酶（CPK）和 CPK-MB 评估、C 反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）、白细胞介素-10（IL-10）和纤溶酶原激活物抑制剂-1（PAI-1）的测定。
异丙肾上腺素诱导的 AMI 导致 ST 段显著抬高，CPK 和 CPK-MB 升高。与对照组相比，AMI 大鼠的 CRP、TNF-α 和血浆 PAI-1 显著升高，而抗炎细胞因子 IL-10 的水平显著降低。在诱导 AMI 之前用阿托伐他汀治疗与血清 CRP、TNF-α、血浆 PAI-1 的降低和血清 IL-10 的增加显著相关。
本研究表明阿托伐他汀作为 AMI 的缓解剂具有一定的应用价值。阿托伐他汀通过降低 PAI-1 水平来恢复促炎和抗炎介质之间的平衡并调节纤溶。
