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Neuroprotective effect of curcumin in middle cerebral artery occlusion induced focal cerebral ischemia in rats

机译:姜黄素对大鼠大脑中动脉阻塞所致局灶性脑缺血的神经保护作用

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Free radical induced neuronal damage is implicated in cerebral ischemia reperfusion (IR) injury and antioxidants are reported to have neuroprotective activity. Several in vitro and in vivo studies have proved the antioxidant potential of curcumin and its metabolites. Hence, in the present study the neuroprotective potential of curcumin was investigated in middle cerebral artery occlusion (MCAO) induced focal cerebral IR injury. 2 h of MCAO and 22 h of reperfusion resulted in the infarct volume of 210.39 +/- 31.25 mm(3). Administration of curcumin 100 and 300 mg/kg, i.p. 30 min. after MCAO produced 37.23 +/- 5.10% and 46.39 +/- 10.23% (P<0.05) reduction in infaret volume, respectively. Ischemia induced cerebral edema was reduced in a dose dependent manner. Curcurnin at 300 mg/kg, i.p. produced 50.96 +/- 6.04% reduction in edema (p < 0.05) volume. Increase in lipid peroxidation after MCAO in ipsilateral and contralateral hemisphere of brain was observed, which was reduced by curcumin (300 mg/kg, i.p.)-treatment. Decrease in superoxide dismutase and glutathione peroxidase activity was observed in ipsilateral hemisphere of MCAO animal. Curcumin-treatment (300 mg/kg, i.p.) prevented IR injury mediated fall in glutathione peroxide activity. Peroxynitrite measured using rhodamine 123 fluorescence and anti-nitrotyrosine immunofluorescence indicated increased peroxynitrite fort-nation after IR insult. Curcumin-treatment reduced peroxynitrite formation and hence the extent of tyrosine nitration in the cytosolic proteins. These results suggest the neuroprotective potential of curcumin in cerebral ischemia and is mediated through its antioxidant activity. (C) 2003 Elsevier Inc. All rights reserved. [References: 50]
机译:自由基诱导的神经元损伤与脑缺血再灌注(IR)损伤有关,据报道抗氧化剂具有神经保护活性。多项体外和体内研究证明姜黄素及其代谢产物具有抗氧化作用。因此,在本研究中,研究了姜黄素在大脑中动脉闭塞(MCAO)引起的局灶性脑IR损伤中的神经保护潜力。 2小时的MCAO和22小时的再灌注导致梗塞体积为210.39 +/- 31.25 mm(3)。给予姜黄素100和300 mg / kg,腹腔注射30分钟。 MCAO后分别减少了37.23 +/- 5.10%和46.39 +/- 10.23%(P <0.05)。缺血引起的脑水肿以剂量依赖性方式降低。姜黄素300 mg / kg,腹腔注射产生的水肿体积减少50.96 +/- 6.04%(p <0.05)。观察到MCAO后大脑同侧和对侧半球脂质过氧化的增加,姜黄素(300 mg / kg,腹腔注射)治疗可减少脂质过氧化。在MCAO动物的同侧半球中观察到超氧化物歧化酶和谷胱甘肽过氧化物酶活性的降低。姜黄素处理(300 mg / kg,腹腔注射)可预防IR损伤介导的谷胱甘肽过氧化物活性下降。使用若丹明123荧光和抗硝基酪氨酸免疫荧光测量的过氧亚硝酸盐表明IR损伤后过氧亚硝酸盐的堡垒增加。姜黄素处理减少了过氧亚硝酸盐的形成,从而减少了胞质蛋白中酪氨酸硝化的程度。这些结果表明姜黄素在脑缺血中的神经保护潜力,并通过其抗氧化活性介导。 (C)2003 Elsevier Inc.保留所有权利。 [参考:50]

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