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首页> 外文期刊>Journal of medicinal food >Behavioral and histologic neuroprotection of aqueous garlic extract after reversible focal cerebral ischemia.
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Behavioral and histologic neuroprotection of aqueous garlic extract after reversible focal cerebral ischemia.

机译:可逆性局灶性脑缺血后大蒜提取物的行为和组织学神经保护作用。

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摘要

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.
机译:本研究的目的是研究大蒜提取物(AGE)对神经行为活性,丙二醛(MDA)和降低的谷胱甘肽(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-转移酶的影响(GST),超氧化物歧化酶(SOD),过氧化氢酶(CAT)和钠钾ATPase(Na(+),K(+)-ATPase)活动以及大脑中动脉(MCA)闭塞中的谷氨酸和天冬氨酸含量( MCAO)大鼠急性脑缺血模型。使用腔内4-0单丝将雄性Wistar大鼠的右MCA闭塞2小时,并允许再灌注22小时。 MCAO导致GSH及其相关酶(GPx,GR和GST)的大量消耗,MDA,谷氨酸和天冬氨酸的显着升高。 MCAO显着降低了Na(+),K(+)-ATPase,SOD和CAT的活性。 MCAO组的神经行为活动(握力,自发运动活动和运动协调)也显着降低。在MCAO诱导前30分钟用AGE(500 mg / mL / kg体重,腹腔注射)预处理可显着减轻缺血诱导的所有改变,并通过减少MCAO和再灌注后神经元细胞死亡与组织病理学密切相关。这些发现表明,AGE有效地调节局灶性局部缺血的神经行为和神经化学变化,这很可能是由于其抗氧化特性。

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