Hamid R Sadeghnia1, Roya Jamshidi2, Amir R Afshari2, Hamid Mollazadeh3, Fatemeh Forouzanfar3, Hasan Rakhshandeh3. 1. Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: sadeghniahr@mums.ac.ir. 2. Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: These data suggest that TCAE exhibits neuroprotection and oligoprotection potential by means of alleviating oxidative stress parameters.
BACKGROUND: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. METHODS: 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. RESULTS: 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. CONCLUSION: These data suggest that TCAE exhibits neuroprotection and oligoprotection potential by means of alleviating oxidative stress parameters.
Authors: Amir R Afshari; Mostafa Karimi Roshan; Mohammad Soukhtanloo; Ahmad Ghorbani; Farzad Rahmani; Mohammad Jalili-Nik; Mohammad Mahdi Vahedi; Azar Hoseini; Hamid R Sadeghnia; Hamid Mollazadeh; Seyed Hadi Mousavi Journal: Avicenna J Phytomed Date: 2019 Jul-Aug
Authors: Amir R Afshari; Mohammad Jalili-Nik; Mohammad Soukhtanloo; Ahmad Ghorbani; Hamid R Sadeghnia; Hamid Mollazadeh; Mostafa Karimi Roshan; Farzad Rahmani; Hamed Sabri; Mohammad Mahdi Vahedi; Seyed Hadi Mousavi Journal: EXCLI J Date: 2019-07-30 Impact factor: 4.068