Department of Surgery, Medical University of Vienna, Vienna, Austria.
Eur J Vasc Endovasc Surg. 2012 Aug;44(2):133-7. doi: 10.1016/j.ejvs.2012.04.020. Epub 2012 Jun 12.
Statins have been reported to suppress the progression of abdominal aortic aneurysm (AAA). However, the effects of statins on inflammatory processes and free radicals generation are poorly understood.
Wall samples from 51 patients (simvastatin patients, n = 34; non-statin patients, n = 17; matched by sex, age and aneurysm size) subjected to elective open AAA repair were analysed. We examined the effects of simvastatin on lipid peroxidation (4-hydroxy-trans-2-nonenal (4-HNE)), hydrogen peroxide (H(2)O(2)), tumour necrosis factor alpha (TNF-α) concentration, superoxide dismutase (SOD) and catalase (CAT) activity as well as nuclear factor kappa B (NF-κB) pathway activation in human AAA wall samples.
Treatment with simvastatin resulted in a decrease in 4-HNE and TNF-α concentration (median 4.18 μg/mg protein vs. 4.75, p = 0.012; median 10.33 pg/ml vs. 11.81, p = 0.026, respectively). CAT activity was higher in the simvastatin group (median 3.98 U ml vs. 3.19, p = 0.023). NF-κB expression was lower (p = 0.018) in the simvastatin group. However, simvastatin had little effect on H(2)O(2) concentration (p = 0.832) and SOD activity (p = 0.401).
Simvastatin inhibits free radicals and TNF-α generation and improves antioxidant capacity of human AAA wall tissue, possibly through the suppression of NF-κB activity. This may be one possible explanation how statins can inhibit AAA oxidative stress.
他汀类药物已被报道可抑制腹主动脉瘤（AAA）的进展。然而，他汀类药物对炎症过程和自由基生成的影响仍知之甚少。
对 51 例接受择期开放 AAA 修复的患者（辛伐他汀组 34 例，非他汀组 17 例，按性别、年龄和动脉瘤大小匹配）的血管壁样本进行分析。我们研究了辛伐他汀对人 AAA 血管壁样本中脂质过氧化（4-羟基-trans-2-壬烯醛（4-HNE））、过氧化氢（H2O2）、肿瘤坏死因子-α（TNF-α）浓度、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性以及核因子 κB（NF-κB）通路激活的影响。
辛伐他汀治疗可降低 4-HNE 和 TNF-α浓度（中位数 4.18μg/mg 蛋白比 4.75，p=0.012；中位数 10.33pg/ml 比 11.81，p=0.026）。辛伐他汀组 CAT 活性更高（中位数 3.98U/ml 比 3.19，p=0.023）。NF-κB 表达较低（p=0.018）。然而，辛伐他汀对 H2O2 浓度（p=0.832）和 SOD 活性（p=0.401）影响较小。
辛伐他汀可抑制自由基和 TNF-α的产生，提高人 AAA 血管壁组织的抗氧化能力，可能是通过抑制 NF-κB 活性。这可能是他汀类药物抑制 AAA 氧化应激的一种可能机制。
