Saleem Sofiyan, Ahmad Muzamil, Ahmad Abdullah Shafique, Yousuf Seema, Ansari Mubeen Ahmad, Khan M Badruzzaman, Ishrat Tauheed, Islam Fakhrul
Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, India.
J Med Food. 2006 Winter;9(4):537-44. doi: 10.1089/jmf.2006.9.537.
The objective of the present study was to investigate the effects of aqueous garlic extract (AGE) on neurobehavioral activities, malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and sodium-potassium ATPase (Na(+),K(+)-ATPase) activities, and glutamate and aspartate content in a middle cerebral artery (MCA) occlusion (MCAO) model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 hours using intraluminal 4-0 monofilament, and reperfusion was allowed for 22 hours. MCAO caused significant depletion in GSH and its dependent enzymes (GPx, GR, and GST) and significant elevation of MDA, glutamate, and aspartate. The activities of Na(+),K(+)- ATPase, SOD, and CAT were decreased significantly by MCAO. The neurobehavioral activities (grip strength, spontaneous motor activity, and motor coordination) were also decreased significantly in the MCAO group. All of the alterations induced by ischemia were significantly attenuated by pretreatment with AGE (500 mg/mL/kg of body weight, i.p.) 30 minutes before the induction of MCAO and correlated well with histopathology by decreasing the neuronal cell death following MCAO and reperfusion. These findings suggest that AGE effectively modulates neurobehavioral and neurochemical changes in focal ischemia, most probably by virtue of its antioxidant properties.
本研究的目的是探讨大蒜水提取物（AGE）对大鼠急性脑缺血大脑中动脉闭塞（MCAO）模型中神经行为活动、丙二醛（MDA）和还原型谷胱甘肽（GSH）水平、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）、谷胱甘肽S-转移酶（GST）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）以及钠钾ATP酶（Na(+)，K(+)-ATPase）活性，还有谷氨酸和天冬氨酸含量的影响。雄性Wistar大鼠的右侧大脑中动脉使用腔内4-0单丝闭塞2小时，然后再灌注22小时。MCAO导致GSH及其相关酶（GPx、GR和GST）显著消耗，MDA、谷氨酸和天冬氨酸显著升高。MCAO使Na(+)，K(+)-ATPase、SOD和CAT的活性显著降低。MCAO组的神经行为活动（握力、自发运动活动和运动协调性）也显著降低。在MCAO诱导前30分钟腹腔注射AGE（500mg/mL/kg体重）预处理可显著减轻缺血诱导的所有改变，并且通过减少MCAO和再灌注后神经元细胞死亡，与组织病理学结果密切相关。这些发现表明，AGE可能凭借其抗氧化特性有效调节局灶性缺血中的神经行为和神经化学变化。
