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首页> 外文期刊>Life sciences >Prevention of kainic acid-induced changes in nitric oxide level and neuronal cell damage in the rat hippocampus by manganese complexes of curcumin and diacetylcurcumin
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Prevention of kainic acid-induced changes in nitric oxide level and neuronal cell damage in the rat hippocampus by manganese complexes of curcumin and diacetylcurcumin

机译：姜黄素和二乙酰姜黄素锰配合物预防海藻酸诱导的大鼠海马一氧化氮水平变化和神经元细胞损伤

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Curcumin is a natural antioxidant isolated from the medicinal plant Curcuma longa Linn. We previously reported that manganese complexes of curcumin (Cp-Mn) and diacetylcurcumin (DiAc-Cp-Mn) exhibited potent superoxide dismutase (SOD)-like activity in an in vitro assay. Nitric oxide (NO) is a free radial playing a multifaceted role in the brain and its excessive production is known to induce neurotoxicity. Here, we examined the in vivo effect of Cp-Mn and DiAc-Cp-Mn on NO levels enhanced by kainic acid (KA) and L-arginine (L-Arg) in the hippocampi of awake rats using a microdialysis technique. Injection of KA (10 mg/kg, i.p.) and L-Arg (1000 mg/kg, i.p.) significantly increased the concentration of NO and Cp-Mn and DiAc-Cp-Mn (50 mg/kg, i.p.) significantly reversed the effects of KA and L-Arg without affecting the basal NO concentration. Following KA-induced seizures, severe neuronal cell damage was observed in the CA1 and CA3 subfields of hippocampal 3 days after KA administration. Pretreatment with Cp-Mn and DiAc-Cp-Mn (50 mg/kg, i.p.) significantly attenuated KA-induced neuronal cell death in both CA1 and CA3 regions of rat hippocampus compared with vehicle control, and Cp-Mn and DiAc-Cp-Mn showed more potent neuroprotective effect than their parent compounds, curcumin and diacetylcurcumin. These results suggest that Cp-Mn and DiAc-Cp-Mn protect against KA-induced neuronal cell death by suppression of KA-induced increase in NO levels probably by their NO scavenging activity and antioxidative activity. Cp-Mn and DiAc-Cp-Mn have an advantage to be neuroprotective agents in the treatment of acute brain pathologies associated with NO-induced neurotoxicity and oxidative stress-induced neuronal damage such as epilepsy, stroke and traumatic brain injury. (c) 2005 Elsevier Inc. All rights reserved.
机译：姜黄素是从药用植物姜黄中分离出的天然抗氧化剂。我们以前报道过，姜黄素（Cp-Mn）和二乙酰姜黄素（DiAc-Cp-Mn）的锰配合物在体外测定中表现出强力的超氧化物歧化酶（SOD）样活性。一氧化氮（NO）是一种自由的放射状分子，在大脑中起着多方面的作用，已知其过量产生会诱发神经毒性。在这里，我们使用微透析技术检查了Cp-Mn和DiAc-Cp-Mn对清醒大鼠海马中海藻酸（KA）和L-精氨酸（L-Arg）增强的NO水平的体内作用。注射KA（10 mg / kg，ip）和L-Arg（1000 mg / kg，ip）可以显着增加NO和Cp-Mn的浓度，而DiAc-Cp-Mn（50 mg / kg，ip）的浓度可以显着逆转。 KA和L-Arg的作用而不会影响基础NO浓度。 KA诱发的癫痫发作后，KA施用3天后，在海马CA1和CA3子区观察到严重的神经元细胞损伤。与媒介物对照相比，用Cp-Mn和DiAc-Cp-Mn（50 mg / kg，ip）预处理可显着减轻KA诱导的大鼠海马CA1和CA3区神经元细胞死亡，以及Cp-Mn和DiAc-Cp-锰比其母体化合物姜黄素和二乙酰姜黄素具有更强的神经保护作用。这些结果表明，Cp-Mn和DiAc-Cp-Mn可能通过抑制KA诱导的NO清除活性和抗氧化活性而抑制KA诱导的NO水平升高，从而防止KA诱导的神经元细胞死亡。 Cp-Mn和DiAc-Cp-Mn具有作为神经保护剂的优势，可用于治疗与NO引起的神经毒性和氧化应激引起的神经元损害（如癫痫，中风和脑外伤）相关的急性脑部疾病。 （c）2005 Elsevier Inc.保留所有权利。

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