Ghoneim Asser I, Abdel-Naim Ashraf B, Khalifa Amani E, El-Denshary Ezzeddin S
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Pharmacol Res. 2002 Sep;46(3):273-9. doi: 10.1016/s1043-6618(02)00123-8.
Oxidative stress is believed to be implicated in the pathogenesis of postischaemic cerebral injury. Many antioxidants were shown to be neuroprotective in experimental models of cerebral ischaemia/reperfusion (I/R). The present study was designed to investigate the potential protective effects of curcumin (CUR) against I/R insult in rat forebrain. The model adopted was that of surgically-induced forebrain ischaemia, performed by means of bilateral common carotid artery occlusion (BCCAO) for 1 h, followed by reperfusion for another 1h. The effects of a single i.p. dose of CUR (50, 100 or 200 mg kg(-1)), administered 0.5 h after the onset of ischaemia, were investigated by assessing oxidative stress-related biochemical parameters in rat forebrain. CUR, at the highest dose level (200 mg kg(-1)), decreased the I/R-induced elevated xanthine oxidase (XO) activity, superoxide anion (O(2)(-)) production, malondialdehyde (MDA) level and glutathione peroxidase (GPx), superoxide dismutase (SOD), and lactate dehydrogenase (LDH) activities. On the other hand, CUR did not affect the declined reduced glutathione (GSH) content due to I/R insult. Worth mentioning is that the activity of catalase (CAT) did not change in response to either I/R insult or drug treatment. In conclusion, CUR was found to protect rat forebrain against I/R insult. These protective effects may be attributed to its antioxidant properties and/or its inhibitory effects on xanthine dehydrogenase/xanthine oxidase (XD/XO) conversion and resultant O(2)(-) production.
氧化应激被认为与缺血性脑损伤的发病机制有关。在脑缺血/再灌注（I/R）实验模型中，许多抗氧化剂已显示出神经保护作用。本研究旨在探讨姜黄素（CUR）对大鼠前脑I/R损伤的潜在保护作用。采用的模型是通过双侧颈总动脉闭塞（BCCAO）1小时，然后再灌注1小时来诱导手术性前脑缺血。在缺血开始后0.5小时给予单次腹腔注射剂量的CUR（50、100或200 mg kg(-1)），通过评估大鼠前脑中与氧化应激相关的生化参数来研究其效果。在最高剂量水平（200 mg kg(-1)）时，CUR降低了I/R诱导升高的黄嘌呤氧化酶（XO）活性、超氧阴离子（O(2)(-)）生成、丙二醛（MDA）水平以及谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD）和乳酸脱氢酶（LDH）的活性。另一方面，CUR并未影响因I/R损伤而降低的还原型谷胱甘肽（GSH）含量。值得一提的是，过氧化氢酶（CAT）的活性在I/R损伤或药物处理后均未发生变化。总之，发现CUR可保护大鼠前脑免受I/R损伤。这些保护作用可能归因于其抗氧化特性和/或对黄嘌呤脱氢酶/黄嘌呤氧化酶（XD/XO）转化及由此产生的O(2)(-)生成的抑制作用。
