Vanderbilt University, Department of Neurology, Nashville, TN 37232, USA.
Neurochem Int. 2012 Jan;60(2):208-12. doi: 10.1016/j.neuint.2011.11.009. Epub 2011 Nov 22.
Stroke is an emerging major health problem often resulting in death or disability. Hyperlipidemia, high blood pressure and diabetes are well established risk factors. Endothelial dysfunction associated with these risk factors underlies pathological processes leading to atherogenesis and cerebral ischemic injury. While mechanisms of disease are complex, endothelial dysfunction involves decreased nitric oxide (NO) and elevated levels of reactive oxygen species (ROS). At physiological levels, ROS participate in regulation of cellular metabolism. However, when ROS increase to toxic levels through imbalance of production and neutralization by antioxidant enzymes, they cause cellular injury in the form of lipid peroxidation, protein oxidation and DNA damage. Central nervous system cells are more vulnerable to ROS toxicity due to their inherent higher oxidative metabolism and less antioxidant enzymes, as well as higher content of membranous fatty acids. During ischemic stroke, ROS concentration rises from normal low levels to a peak point during reperfusion possibly underlying apoptosis or cellular necrosis. Clinical trials and animal studies have shown that natural compounds can reduce oxidative stress due to excessive ROS through their antioxidant properties. With further study, we may be able to incorporate these compounds into clinical use with potential efficacy for both the treatment and prevention of stroke.
中风是一个新兴的主要健康问题，通常导致死亡或残疾。高血脂、高血压和糖尿病是公认的危险因素。与这些危险因素相关的内皮功能障碍是导致动脉粥样硬化和脑缺血损伤的病理过程的基础。虽然疾病的机制很复杂，但内皮功能障碍涉及一氧化氮（NO）减少和活性氧（ROS）水平升高。在生理水平上，ROS 参与细胞代谢的调节。然而，当 ROS 通过抗氧化酶的产生和中和失衡而增加到毒性水平时，它们会以脂质过氧化、蛋白质氧化和 DNA 损伤的形式引起细胞损伤。中枢神经系统细胞由于其固有的较高氧化代谢和较少的抗氧化酶，以及较高的膜脂肪酸含量，更容易受到 ROS 毒性的影响。在缺血性中风中，ROS 浓度从正常的低水平上升到再灌注期间的峰值，这可能是细胞凋亡或坏死的基础。临床试验和动物研究表明，天然化合物可以通过其抗氧化特性减少过多 ROS 引起的氧化应激。随着进一步的研究，我们也许能够将这些化合物纳入临床应用，为中风的治疗和预防提供潜在的疗效。
