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Protective effects of Phoenix dactylifera against oxidative stress and neuronal damage induced by global cerebral ischemia in rats

机译:凤梨对全脑缺血所致氧化应激和神经元损伤的保护作用

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摘要

Phoenix dactylifera (PD) has been claimed for its neuroprotective potential in the traditional system of medicine but has not yet been scientifically documented. Phytochemical reports of Phoenix dactylifera fruits have demonstrated the presence of polyphenols and flavonoids, which have already been documented to play major role in neuroprotection against various experimental models of cerebral ischemia/reperfusion. In the present study, we have investigated the neuroprotective as well as antioxidant properties of methanolic extract of Phoenix dactylifera fruits (MEPD) at 30, 100, 300 mg/kg p.o against global cerebral ischemia-induced oxidative stress and neuronal death. The global cerebral ischemia was induced by occlusion of bilateral common carotid arteries for 5 min followed by 24 h of reperfusion. Varied biochemical/enzymatic alterations, produced subsequent to the application bilateral common carotid artery occlusion (BCCAO) followed by reperfusion viz. increase in lipid peroxidation and decrease in glutathione, glutathione reductase, catalase, glutathione-S-transferase, glutathione peroxidase and superoxide dismutase, were markedly reversed and restored to near normal levels in the groups pre-treated with 15 days. The pretreatment also reversed the histopathological changes induced by global cerebral ischemia in CA1 hippocampal region. The protective action, exhibited by MEPD against global cerebral induced brain injury, suggests its therapeutic potential in cerebrovascular diseases (CVD) including stroke. These findings are important because the present treatment strategies for CVD are far from adequate and PD with wide usage is known to be a safe natural product.
机译:Phoenix dactylifera(PD)因其在传统医学系统中具有神经保护作用而备受称赞,但尚未得到科学证明。 Phoenix dactylifera果实的植物化学报告显示,多酚和类黄酮的存在已被证明在针对脑缺血/再灌注的各种实验模型的神经保护中起主要作用。在本研究中,我们研究了凤凰果(Phoenix dactylifera)果实(MEPD)甲醇提取物在30、100、300 mg / kg p.o的抗神经保护性和抗氧化性,以对抗整体性脑缺血引起的氧化应激和神经元死亡。通过阻塞双侧颈总动脉5分钟,然后再灌注24小时,诱发全脑缺血。在应用双侧颈总动脉闭塞(BCCAO)后再灌注后产生各种生物化学/酶学改变。在15天的预处理组中,脂质过氧化的增加和谷胱甘肽,谷胱甘肽还原酶,过氧化氢酶,谷胱甘肽S-转移酶,谷胱甘肽过氧化物酶和超氧化物歧化酶的减少被显着逆转并恢复到接近正常水平。预处理还逆转了CA1海马区全脑缺血引起的组织病理学变化。 MEPD对全脑诱发的脑损伤具有保护作用,表明其在包括中风在内的脑血管疾病(CVD)中具有治疗潜力。这些发现很重要,因为当前的CVD治疗策略还远远不够,而且广泛使用的PD是一种安全的天然产品。

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