Medical School of Dicle University, Department of Cardiovascular Surgery, 21280, Diyarbakir, Turkey.
CNS Neurol Disord Drug Targets. 2013 Nov;12(7):1011-6. doi: 10.2174/18715273113129990085.
Ischemia reperfusion injuries can be threatening to end organ viability and can progress, with mortal and morbid outcomes. In particular, neural tissues are highly sensitive to hypoxia and reperfusion stress. This study aimed to determine the neuroprotective effects of rosuvastatin on spinal cord ischemia reperfusion injury. Forty male Sprague- Dawley rats were divided into four equal groups: group I (control), group II (sham with simple laparotomy), group III (ischemia-reperfusion), group IV (ischemia-reperfusion group with continuous rosuvastatin utilization), and group V (ischemia-reperfusion group with rosuvastatin-withdrawal after reperfusion). Spinal cord ischemia was induced by clamping the aorta below the left renal artery and above the aortic bifurcation. Reperfusion was provided after 72(nd) hours of ischemia. After reperfusion, blood samples and spinal cord tissue samples were taken from all the rats. Oxidative and antioxidant markers from both serum and tissue samples were evaluated, and tissues were examined histopathologically. There were no significant differences between the control and sham groups. A notable increase in oxidative markers was observed in group III compared to group I. In addition, a significant decrease in antioxidant markers was detected in group III. However, there was a marked preservation in the tissue and blood samples of groups IV and V compared to group III in terms of oxidative damage. Additionally, definitive prophylaxes were seen in the histopathological examination of the tissue samples in groups IV and V compared with group III. These significant findings show that rosuvastatin has a considerable protective effect on neural tissue against oxidative damage. Likewise, the early withdrawal of rosuvastatin has a clear neuroprotective effect similar to that of continuous therapy. Nevertheless, other systematic effects and beneficial neural effects of statins should be investigated in further clinical trials.
缺血再灌注损伤可能对终末器官的存活构成威胁，并可能进展为致命和致残的后果。特别是神经组织对缺氧和再灌注应激高度敏感。本研究旨在确定瑞舒伐他汀对脊髓缺血再灌注损伤的神经保护作用。将 40 只雄性 Sprague-Dawley 大鼠随机分为四组：I 组（对照组）、II 组（单纯剖腹术假手术组）、III 组（缺血再灌注组）、IV 组（缺血再灌注组+再灌注后持续瑞舒伐他汀治疗组）和 V 组（缺血再灌注组+再灌注后瑞舒伐他汀撤药组）。通过夹闭左肾动脉下方和主动脉分叉上方的主动脉来诱导脊髓缺血。缺血 72 小时后再灌注。再灌注后，从所有大鼠中抽取血液样本和脊髓组织样本。评估血清和组织样本中的氧化和抗氧化标志物，并进行组织病理学检查。对照组和假手术组之间无显著差异。与 I 组相比，III 组的氧化标志物显著增加。此外，III 组的抗氧化标志物显著减少。然而，与 III 组相比，IV 组和 V 组的组织和血液样本中的氧化损伤明显得到保留。此外，与 III 组相比，IV 组和 V 组的组织样本的组织病理学检查显示出明确的预防作用。这些显著的发现表明，瑞舒伐他汀对神经组织具有显著的抗氧化损伤保护作用。同样，早期撤药瑞舒伐他汀对神经组织具有与持续治疗相似的明确神经保护作用。然而，应该在进一步的临床试验中研究他汀类药物的其他系统作用和有益的神经作用。
