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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Attenuation of rat ischemic brain damage by aged garlic extracts: a possible protecting mechanism as antioxidants.
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Attenuation of rat ischemic brain damage by aged garlic extracts: a possible protecting mechanism as antioxidants.

机译：老化的大蒜提取物可减轻大鼠缺血性脑损伤：作为抗氧化剂的一种可能的保护机制。

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Effects of an aged garlic extract and its thioallyl components on rat brain ischemia were examined using a middle cerebral artery occlusion model and a transient global ischemia model. In focal ischemia, an aged garlic extract, S-allyl cysteine (SAC), Allyl sulfide (AS) or Allyl disulfide (ADS) was administered 30 min prior to ischemic insult. Three days after ischemic insult, water contents of both ischemic and contralateral hemispheres were measured to assess the degree of ischemic damage. The water content of the ischemic control (no drug treatment) group was 81.50 +/- 0.07% (mean +/- SEM). It was significantly reduced with the administration of 300 mg/kg of SAC; the water content was 80.66 +/- 0.11% (P < 0.001). The histological observation using 2,3,5-triphenyltetrazolium chloride staining demonstrated that the administration of SAC reduced infarct volume. Neither AS nor ADS was effective. In global ischemia, the production of reactive oxygen species (ROS) was measured ex vivo using a spin-trapping agent, alpha-phenyl-N-tert-butylnitrone, and electron paramagnetic resonance spectroscopy. The production of ROS had two peaks; first at 5 min and second at 20 min after reperfusion. Both SAC and 7-nitro indazole, a nitric oxide synthase inhibitor, did not attenuate the amount of ROS produced at the first peak, but did the amount of the second peak. A possible involvement of peroxinitrite, which may be formed from superoxide and nitric oxide and is known to be highly toxic in ischemia/reperfusion injury of the brain, was suggested.
机译：使用大脑中动脉闭塞模型和短暂性全局缺血模型检查了衰老的大蒜提取物及其硫代烯丙基成分对大鼠脑缺血的影响。在局灶性缺血中，在缺血性损伤前30分钟给予老化的大蒜提取物，S-烯丙基半胱氨酸（SAC），烯丙基硫（AS）或烯丙基二硫（ADS）。缺血性损伤后三天，测量缺血性和对侧半球的水含量以评估缺血性损伤的程度。缺血对照组（无药物治疗）组的水含量为81.50 +/- 0.07％（平均值+/- SEM）。通过服用300 mg / kg的SAC可以显着降低该剂量;水分含量为80.66 +/- 0.11％（P <0.001）。使用2,3,5-三苯基四唑氯化物染色的组织学观察表明，SAC的使用减少了梗塞体积。 AS和ADS均无效。在全球缺血中，使用自旋捕集剂，α-苯基-N-叔丁基硝酮和电子顺磁共振光谱离体测量了活性氧（ROS）的产生。 ROS的产生有两个峰值。第一次在再灌注后5分钟，第二次在20分钟后。 SAC和一氧化氮合酶抑制剂7-硝基吲唑都没有减弱在第一个峰上产生的ROS的数量，但是在第二个峰上却有所减弱。建议过氧化亚铁可能参与其中，它可能由超氧化物和一氧化氮形成，并且已知在脑缺血/再灌注损伤中具有高毒性。

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