姜黄素新型吡唑衍生物CNB-001的体外抗氧化能力和脱氧核糖核酸保护活性

Richard L. Jayaraj, N. Elangovan
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引用次数: 4

摘要

背景:在许多神经退行性疾病中,自由基被认为是引发一系列毒性事件的基础,导致氧化应激和细胞死亡。如今,除了药物的作用方式外,抗氧化剂已成为治疗各种疾病的强制性药物。CNB-001是由姜黄素和环己基双酚a合成的一种新型杂化分子,具有多种生物活性,但其抗氧化性能尚未得到明确的研究。目的:通过体外抗氧化实验分析CNB-001对各种自由基的清除能力,并评价脱氧核糖核酸(DNA)对CNB-001抗羟基自由基的保护能力。材料与方法:采用光谱学方法分析CNB-001对DPPH、ABTS、一氧化氮、超氧化物、过氧化氢、超氧阴离子、羟基、过氧化氢自由基的清除能力和还原能力,评价其体外抗氧化能力。采用标准琼脂糖凝胶电泳法对羟基自由基作用下的pUC19质粒DNA进行了DNA保护活性评价。结果:观察到CNB-001对自由基的清除作用呈剂量依赖性。CNB-001对2,2-二苯基-1-吡啶肼基(IC50 = 44.99 μg/ml)、2,2-氮唑(3-乙基苯并噻唑-6-磺酸)(IC50 = 17.99 μg/ml)、一氧化氮(IC50 = 1.36 μg/ml)、超氧化物(IC50 = 77.17 μg/ml)、过氧化氢(IC50 = 492.7 μg/ml)、超氧化物(IC50 = 36.92 μg/ml)和羟基(IC50 = 456.5 μg/ml)自由基均有较强的清除能力,还原能力为11.53 μg/ml。CNB-001对•OH引起的质粒DNA (pUC19)链断裂具有明显的保护作用,且呈剂量依赖性。结论:CNB-001具有良好的抗氧化活性,可降低活性氧和活性氮自由基,对羟基自由基的DNA断裂具有明显的保护作用。因此,CNB-001可以作为自由基诱导的神经退行性疾病的潜在药物进一步开发。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
In vitro antioxidant potential and deoxyribonucleic acid protecting activity of CNB-001, a novel pyrazole derivative of curcumin
Background: Free radicals are underpinned to initiate cascade of toxic events leading to oxidative stress and resultant cell death in many neurodegenerative disorders. Now-a-days antioxidants have become mandatory in the treatment of various diseases apart from the drug's modes of action. CNB-001, a novel hybrid molecule synthesized by combining curcumin and cyclohexyl bisphenol A is known to possess various biological activities, but the antioxidative property of the compound has not yet been elucidated. Aim: The present study is aimed to analyze various free radicals scavenging by employing in vitro antioxidant assays and to evaluate the deoxyribonucleic acid (DNA) protecting the ability of CNB-001 against hydroxyl radicals. Materials and methods: The in vitro antioxidant potential of CNB-001 was evaluated by analyzing its ability to scavenge DPPH, ABTS, nitric oxide, superoxide, hydrogen peroxide, superoxide anion, hydroxyl, hydrogen peroxide radicals and reducing power using spectroscopic method. The DNA protecting activity of CNB-001 was also evaluated on pUC19 plasmid DNA subjected to hydroxyl radicals using standard agarose gel electrophoresis. Results: From the assays, it was observed that CNB-001 scavenged free radicals effectively in a dose dependent manner. CNB-001 scavenged 2,2-diphenyl-1-picrylhydrazyl (IC50 = 44.99 μg/ml), 2,2-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) (IC50 = 17.99 μg/ml), nitric oxide (IC50 = 1.36 μg/ml), superoxide radical (IC50 = 77.17 μg/ml), hydrogen peroxide (IC50 = 492.7 μg/ml), superoxide (IC50 = 36.92 μg/ml) and hydroxyl (IC50 = 456.5 μg/ml) radicals effectively and the reducing power was found to be 11.53 μg/ml. CNB-001 showed considerable protecting activity against plasmid DNA (pUC19) strand scission by •OH at dose dependent manner. Conclusion: Results from these assays concluded that CNB-001 has a good antioxidant potential by reducing reactive oxygen and reactive nitrogen radicals and it showed significant protecting activity against DNA scission by hydroxyl radicals. Hence, CNB-001 can be further developed as potential drug for free radical induced neurodegenerative disorders.
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