Sadeghnia Hamid R, Jamshidi Roya, Afshari Amir R, Mollazadeh Hamid, Forouzanfar Fatemeh, Rakhshandeh Hasan
Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mult Scler Relat Disord. 2017 May;14:60-67. doi: 10.1016/j.msard.2017.03.012. Epub 2017 Apr 5.
Quinolinic acid (QA) is a product of tryptophan degradation and its pathologic accumulation has been found to induce neuroinflammatory and demyelinating diseases such as multiple sclerosis via excessive free radicals generation. Recent studies showed that Terminalia chebula has several pharmacological effects such as antioxidant, anti-inflammatory and neuroprotective properties. The aim of this study was evaluation of the protective effect of T. chebula alcoholic extract (TCAE) on oxidative PC12 and OLN-93 cells death induced by QA.
The cells were pretreated with TCAE (6.25-50μg/mL) for 2h and then subjected to QA (8mM) for 24h. Cell viability and the parameters of redox status including the levels of intracellular reactive oxygen species (ROS), lipid peroxidation and oxidative DNA damage were measured using 2-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT), 2,7-dicholorofluorecin diacetate (DCF-DA), thiobarbituric acid and comet assays, respectively.
Based on Folin-Ciocalteu method, the total phenolic compounds in TCAE were estimated about 1.18%. TCAE at concentration ranges of 6.25-50μg/mL had no toxic effect on cell viability (p>0.05). Treatment with TCAE significantly increased cell viability following QA insult at concentrations above 25μg/mL (p<0.01). Cytoprotective potential of TCAE also ameliorated ROS accumulation, lipid peroxidation and DNA damage induced by QA.
These data suggest that TCAE exhibits neuroprotection and oligoprotection potential by means of alleviating oxidative stress parameters.
喹啉酸（QA）是色氨酸降解产物，其病理性蓄积可通过产生过量自由基诱导神经炎症和脱髓鞘疾病，如多发性硬化症。最近的研究表明，诃子具有抗氧化、抗炎和神经保护等多种药理作用。本研究旨在评估诃子醇提取物（TCAE）对QA诱导的氧化型PC12和OLN-93细胞死亡的保护作用。
细胞先用TCAE（6.25-50μg/mL）预处理2小时，然后用QA（8mM）处理24小时。分别使用2-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐（MTT）、2,7-二氯荧光素二乙酸酯（DCF-DA）、硫代巴比妥酸和彗星试验检测细胞活力以及氧化还原状态参数，包括细胞内活性氧（ROS）水平、脂质过氧化和氧化DNA损伤。
基于福林-西奥尔特法，TCAE中的总酚类化合物估计约为1.18%。浓度范围为6.25-50μg/mL的TCAE对细胞活力无毒性作用（p>0.05）。在浓度高于25μg/mL时，用TCAE处理可显著提高QA损伤后的细胞活力（p<0.01）。TCAE的细胞保护潜力还改善了QA诱导的ROS积累、脂质过氧化和DNA损伤。
这些数据表明，TCAE通过减轻氧化应激参数表现出神经保护和少突胶质细胞保护潜力。
