Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models
Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models
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DOI：
10.1007/s12640-018-9926-y
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发表时间：
2018-10-01
影响因子：
3.7
通讯作者：
Santamaria, Abel
中科院分区：
文献类型：
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作者：
Colonnello, Aline;Kotlar, Ilan;Santamaria, Abel
表现出抗氧化剂，神经保护和调节特性的天然产品所固有的人类正在获得关注的生物医学研究。阿魏酸（FA）是一种具有抗氧化和细胞保护作用的酚类化合物。它存在于几种蔬菜中，包括甘蔗，它是主要的抗氧化剂成分。在这里，我们比较了抗氧化剂和细胞保护作用的FA与甘蔗水提取物（SCAE）。具体而言，我们评估了大鼠大脑皮层切片中细胞功能障碍的生化标志物和秀丽隐杆线虫中生理应激的标志物，暴露于毒素后引起不同的神经毒性机制，包括直接氧化应激和/或兴奋性毒性。在大鼠皮层切片，FA（250和500 μ M），但不是SCAE（类似于270 μ M的总多酚），防止由兴奋毒素喹啉酸（QUIN，100 μ M），促氧化剂硫酸亚铁（FeSO 4，25 μ M），和多巴胺能促氧化剂6-羟基多巴胺（6-OHDA，100 μ M）诱导的还原能力的损失。野生型（N2）C. FA（38 mM）对FeSO 4（15 mM）和6-OHDA（25 mM）诱导的存活率降低以及QUIN（100 mM）、FeSO 4和6-OHDA诱导的运动改变具有保护作用。相比之下，SCAE（类似于13.5 mM的总多酚）诱发的保护作用，减少生存诱导的三种有毒物质，运动改变诱导的FeSO 4，和生殖缺陷诱导的FeSO 4。此外，FA不能逆转所有这些毒素在skn-1（-/-）菌株（VC 1772）中诱导的存活率降低，该菌株缺乏哺乳动物Nrf 2的同源物，一种主抗氧化基因。总之，我们的研究结果表明：（1）FA和SCAE都提供了对毒性条件的保护，（2）并非SCAE固有的所有作用都是由于FA，（3）FA需要skn-1途径在C中发挥其保护作用。优雅
Molecules exhibiting antioxidant, neuroprotective, and regulatory properties inherent to natural products consumed by humans are gaining attention in biomedical research. Ferulic acid (FA) is a phenolic compound possessing antioxidant and cytoprotective properties. It is found in several vegetables, including sugarcane, where it serves as the main antioxidant component. Here, we compared the antioxidant and cytoprotective effects of FA with those of the total sugarcane aqueous extract (SCAE). Specifically, we assessed biochemical markers of cell dysfunction in rat cortical brain slices and markers of physiological stress in Caenorhabditis elegans upon exposure to toxins evoking different mechanisms of neurotoxicity, including direct oxidative stress and/or excitotoxicity. In rat cortical slices, FA (250 and 500 mu M), but not SCAE (similar to 270 mu M of total polyphenols), prevented the loss of reductive capacity induced by the excitotoxin quinolinic acid (QUIN, 100 mu M), the pro-oxidant agent ferrous sulfate (FeSO4, 25 mu M), and the dopaminergic pro-oxidant 6-hydroxydopamine (6-OHDA, 100 mu M). In wild-type (N2) C. elegans, FA (38 mM) exerted protective effects on decreased survival induced by FeSO4 (15 mM) and 6-OHDA (25 mM), and the motor alterations induced by QUIN (100 mM), FeSO4, and 6-OHDA. In contrast, SCAE (similar to 13.5 mM of total polyphenols) evoked protective effects on the decreased survival induced by the three toxic agents, the motor alterations induced by FeSO4, and the reproductive deficit induced by FeSO4. In addition, FA was unable to reverse the decreased survival induced by all these toxins in the skn-1(-/-) strain (VC1772), which lacks the homolog of mammalian Nrf2, a master antioxidant gene. Altogether, our results suggest that (1) both FA and SCAE afford protection against toxic conditions, (2) not all the effects inherent to SCAE are due to FA, and (3) FA requires the skn-1 pathway to exert its protective effects in C. elegans.