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染料木黄酮对大鼠局灶性脑缺血损伤发挥神经保护作用。

Genistein exerts neuroprotective effect on focal cerebral ischemia injury in rats.

机构信息

Department of Neurosurgery, Faculty of Medicine, Canakkale Onsekiz Mart University, Canakkale, Turkey,

出版信息

Inflammation. 2015;38(3):1311-21. doi: 10.1007/s10753-014-0102-0.

DOI:10.1007/s10753-014-0102-0
PMID:25567369
Abstract

Brain ischemia and treatment are one of the important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most important causes of damage. Currently, there are studies on many chemopreventive agents to prevent cerebral ischemia damage. Our aim is to research the preventive effect of the active ingredient in genistein, previously unstudied, on oxidative damage in cerebral ischemia. Rats were randomly divided into three groups: control group (no medication or surgical procedure), ischemia group, and artery ischemia+genistein group, sacrificed at 24 h after ischemia. The harvested brain tissue from the right hemisphere was investigated histopathologically and for tissue biochemistry. Superoxide dismutase and nuclear respiratory factor 1 values decreased after ischemia and they increased after genistein treatment, while increased malondialdehyde levels after ischemia reduced after treatment. Apoptosis-related cysteine peptidase caspase-3 and caspase-9 values increased after ischemia, but reduced after treatment. Our study revealed that genistein treatment in cerebral ischemia reduced oxidative stress and neuronal degeneration. We believe that genistein treatment may be an alternative treatment method.

摘要

脑缺血及其治疗是神经科学的重要课题之一。目前认为,缺血后形成的自由基和炎症是造成损伤的最重要原因。已有许多化学预防剂用于研究,以防止脑缺血损伤。我们的目的是研究之前未研究过的染料木黄酮的活性成分对脑缺血氧化损伤的预防作用。大鼠随机分为三组:对照组(无药物或手术)、缺血组和动脉缺血+染料木黄酮组,缺血后 24 小时处死。右半脑组织行组织病理学和组织生物化学检查。缺血后超氧化物歧化酶和核呼吸因子 1 值降低,染料木黄酮治疗后增加,而缺血后丙二醛水平升高,治疗后降低。缺血后与细胞凋亡相关的半胱氨酸肽酶 caspase-3 和 caspase-9 值增加,但治疗后减少。我们的研究表明,脑缺血时染料木黄酮治疗可减轻氧化应激和神经元变性。我们认为,染料木黄酮治疗可能是一种替代治疗方法。

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Selenium preserves mitochondrial function, stimulates mitochondrial biogenesis, and reduces infarct volume after focal cerebral ischemia.硒能保护线粒体功能,刺激线粒体生物发生,减少局灶性脑缺血后的梗死体积。
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Neuroprotection by the soy isoflavone, genistein, via inhibition of mitochondria-dependent apoptosis pathways and reactive oxygen induced-NF-κB activation in a cerebral ischemia mouse model.
天然产物类药物:针对神经退行性病变的潜在药物靶点。
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Therapeutic Potential and Mechanisms of Novel Simple O-Substituted Isoflavones against Cerebral Ischemia Reperfusion.新型简单 O-取代异黄酮类化合物治疗脑缺血再灌注的潜力及机制。
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Neuronal GPER Participates in Genistein-Mediated Neuroprotection in Ischemic Stroke by Inhibiting NLRP3 Inflammasome Activation in Ovariectomized Female Mice.神经元 GPER 通过抑制 NLRP3 炎性小体激活参与缺血性脑卒中后 Genistein 的神经保护作用。
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