Celastrus paniculatus seed oil and organic extracts attenuate hydrogen peroxide- and glutamate-induced injury in embryonic rat forebrain neuronal cells
Celastrus paniculatus seed oil and organic extracts attenuate hydrogen peroxide- and glutamate-induced injury in embryonic rat forebrain neuronal cells
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DOI：
10.1016/j.phymed.2003.11.011
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发表时间：
2006-01-01
期刊：
影响因子：
7.9
通讯作者：
Doctor, BP
中科院分区：
文献类型：
--
作者：
Godkar, PB;Gordon, RK;Doctor, BP
苦皮藤种子油据报道，CP具有改善记忆的作用，CP的甲醇提取物(ME)在人非永生化成纤维细胞中具有清除自由基和抗氧化的作用。在本研究中，我们研究了CP种子油(CPO)及其两种提取物--乙醇提取物(EE)和ME的清除自由基能力。CPO和EE显示出剂量依赖的清除自由基的能力，但程度低于ME。氧化应激涉及自由基的产生，清除自由基是神经保护的机制之一。因此，我们研究了CPO、ME和EE对过氧化氢(H_2O_2)和谷氨酸诱导的胚胎大鼠前脑神经细胞(FBNC)神经毒性的保护作用。CPO对神经细胞的预处理呈剂量依赖性地减轻过氧化氢诱导的神经元死亡。ME和EE可部分减轻H_2O_2诱导的毒性，但对神经元存活的作用不如CPO。在过氧化氢处理的细胞中，超氧化物歧化酶(SOD)活性未受影响，但过氧化氢酶(CAT)活性降低，丙二醛(MDA)水平升高。CPO、ME或EE预处理显著提高了过氧化氢酶活性，降低了丙二醛水平。此外，CPO预处理可剂量依赖性地减轻谷氨酸诱导的神经元死亡。细胞内乙酰胆碱酯酶(AChE)活性不受CPO、ME或EE的影响，提示CPO的神经保护作用不依赖于AChE活性的变化。综上所述，这些数据表明，CPO、ME和EE保护神经细胞免受过氧化氢诱导的毒性，部分原因是它们的抗氧化性能，以及它们诱导抗氧化酶的能力。然而，抗氧化性最差的CPO在防止过氧化氢和谷氨酸诱导的神经细胞毒性方面最有效。因此，除了清除自由基属性。CP种子成分(CP-C)的神经保护作用机制有待阐明。(C)2005年爱思唯尔·格林布赫。版权所有。
Seed oil of Celastrus paniculatus Willd. (CP) has been reported to improve memory and the methanolic extract (ME) of CP was shown to exhibit free-radical-scavenging properties and anti-oxidant effects in human non-immortalized fibroblasts. In the present study, we have investigated the free-radical-scavenging capacity of CP seed oil (CPO) and two extracts, an ethanolic extract (EE) and a ME. CPO and EE showed dose-dependent, free-radical-scavenging capacity, but to a lesser degree than observed for ME. Oxidative stress involves the generation of free radicals and free radical scavenging is one of the mechanisms of neuroprotection. We therefore investigated the effects of CPO, ME, and EE for protection against hydrogen peroxide (H2O2)- and glutamate-induced neurotoxicity in embryonic rat forebrain neuronal cells (FBNC). Pretreatment of neuronal cells with CPO dose-dependently attenuated H2O2-induced neuronal death. Pre-treatment with ME and EE partially attenuated H2O2-induced toxicity, but these extracts were less effective than CPO for neuronal survival. In H2O2-treated cells, cellular superoxide dismutase (SOD) activity was unaffected, but catalase activity was decreased and levels of malondialdehyde (MDA) were increased. Pre-treatment with CPO, ME, or EE increased catalase activity and decreased MDA levels significantly. Also, CPO pre-treatment attenuated glutamate-induced neuronal death dose-dependently. The activity of cellular acetylcholinesterase (AChE) was not affected by CPO, ME, or EE, suggesting that the neuroprotection offered by CPO was independent of changes in AChE activity. Taken together, the data suggest that CPO, ME, and EE protected neuronal cells against H2O2-induced toxicity in part by virtue of their antioxidant properties, and their ability to induce antioxidant enzymes. However, CPO, which exhibited the least antioxidant properties, was the most effective in preventing neuronal cells against H2O2- and glutamate-induced toxicities. Thus, in addition to free-radical scavenging attributes. the mechanism of CP seed component (CP-C) neuroprotection must be elucidated. (c) 2005 Elsevier GrnbH. All rights reserved.