Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, 110062, India.
Neurochem Res. 2011 Aug;36(8):1360-71. doi: 10.1007/s11064-011-0458-6. Epub 2011 Apr 7.
Experimental studies have demonstrated that oxidative stress and apoptosis play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The purpose of this study was to determine whether the quercetin dihydrate (Q) protects against cerebral ischemia neuronal damage. Male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h and reperfused for 72 h. Quercetin (30 mg/kg, i.p) was administrated 30 min before the onset of ischemia and after the ischemia at interval of 0, 24, 48, and 72 h. The administration of Q showed marked reduction in infarct size, reduced the neurological deficits in terms of behaviors, suppressed neuronal loss and diminished the p53 expression in MCAO rats. Q was found to be successful in upregulating the antioxidant status and lowering the TBARS level. Conversely, the elevated activity of poly (ADP-ribose) polymerase (PARP), and activity of caspase-3 in MCAO group was attenuated significantly in Q treated group when compared with MCAO group. Our study reveals that Q, as a powerful antioxidant, could prevent free radicals associated oxidative damage and morphological changes in the MCAO rats. Thus, it may have a therapeutic value for the treatment of stroke.
实验研究表明，氧化应激和细胞凋亡在脑缺血发病机制中起重要作用，可能成为治疗的靶点。本研究旨在确定二水槲皮素（Q）是否对脑缺血神经元损伤具有保护作用。雄性 Wistar 大鼠接受短暂性大脑中动脉闭塞（MCAO）2 小时，再灌注 72 小时。Q（30mg/kg，腹腔注射）在缺血前 30 分钟和缺血后每隔 0、24、48 和 72 小时给予。Q 的给药显著减少梗死面积，降低行为学上的神经功能缺损，抑制 MCAO 大鼠的神经元丢失和减少 p53 表达。Q 成功地上调了抗氧化状态并降低了 TBARS 水平。相反，与 MCAO 组相比，Q 处理组中聚（ADP-核糖）聚合酶（PARP）的活性和 caspase-3 的活性显著降低。我们的研究表明，Q 作为一种强大的抗氧化剂，可以防止自由基相关的氧化损伤和 MCAO 大鼠的形态变化。因此，它可能对治疗中风具有治疗价值。
