Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia
Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia
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DOI：
10.5772/32933
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发表时间：
2012-03
影响因子：
5
通讯作者：
Naohiro Iwata;M. Okazaki;R. Nakano;Chisato Kasahara;S. Kamiuchi;Fumiko Suzuki;H. Iizuka;Hirokazu Matsuzaki;Yasuhide Hibino
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文献类型：
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作者：
Naohiro Iwata;M. Okazaki;R. Nakano;Chisato Kasahara;S. Kamiuchi;Fumiko Suzuki;H. Iizuka;Hirokazu Matsuzaki;Yasuhide Hibino
糖尿病是一种代谢紊乱，全世界有数亿人患有，其特征在于由胰岛素分泌和/或作用不足引起的高血糖症（Wild等人，2004年）。与糖尿病相关的并发症影响血管、眼睛、肾脏和周围神经，降低糖尿病患者的生活质量。此外，糖尿病被广泛认为是动脉粥样硬化疾病如急性脑缺血的主要危险因素。事实上，与非糖尿病患者相比，糖尿病患者具有更高的中风风险（Baynes 1991; Stephens等人，2009年）。此外，他们更可能具有不良预后和中风后增加的死亡率（Biller等人，1993; Vinik等人，2002年）。先前的研究已经证明，糖尿病状态增加了脑中的氧化应激并加重了I型和II型中的脑缺血性损伤（Li等人，2004; Saito等人，2005; Rizk等人，2005）和II型糖尿病动物模型（Anabela等人，2006; Tureyen等人，2011年）。除了归因于缺血核心区域中血管阻塞引起的缺氧和ATP消耗的神经元损伤之外，由随后的再灌注引起的脑损伤也涉及短暂缺血的病理生理学（Doyle等人，2008; Nakka等人，2008; Wang等人，2010年）。在再灌注期间，活性氧物质（ROS）和活性氮物质（RNS）的产生通过突然再充氧而增强（Cuzzocrea等人，2001; Saito等人，2005年）。除了对细胞膜、蛋白质和DNA的直接损伤作用外，
Diabetes mellitus is a metabolic disorder, suffered by hundreds of millions of people throughout the world, which is characterized by hyperglycemia resulting from insufficiency of insulin secretion and/or action (Wild et al., 2004). Complications associated with diabetes affecting vessels, eyes, kidney, and peripheral nerves reduce the QOL of diabetic patients. Also, diabetes is widely recognized as a major risk factor for atherosclerotic disease such as acute brain ischemia. Indeed, diabetic patients have a higher risk of stroke compared with non-diabetic patients (Baynes 1991; Stephens et al., 2009). Additionally, they are more likely to have a poor prognosis and increased mortality after stroke (Biller et al., 1993; Vinik et al., 2002). Previous studies have demonstrated that the diabetic state increases oxidative stress in the brain and aggravates cerebral ischemic injury in both type I (Li et al., 2004; Saito et al., 2005; Rizk et al., 2005) and type II diabetic animal models (Anabela et al., 2006; Tureyen et al., 2011). In addition to neuronal damage attributed to hypoxia and ATP depletion caused by vascular obstruction in ischemic core region, cerebral injury caused by subsequent reperfusion is also involved in the pathophysiology of transient ischemia (Doyle et al., 2008; Nakka et al., 2008; Wang et al., 2010). During reperfusion, the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is enhanced by abrupt re-oxygenation (Cuzzocrea et al., 2001; Saito et al., 2005). Besides direct injurious effects to the cell membrane, proteins and DNA by