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      Investigation of the neuroprotective effects of a novel synthetic compound via the mitochondrial pathway

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          Abstract

          The present study aimed to investigate the neuroprotective effect of a novel synthetic compound (5zou) on differentiated PC12 cells against 6-hydroxydopamine (6-OHDA) and L-glutamic acid (L-Glu) neurotoxin-induced cell injury and the potential mechanisms involved. 5zou is a 2, 2-disubstituted 1,2-dihydropyridine. PC12 cells were treated with 6-OHDA and L-Glu to establish neurotoxic cell models. MTT assay, DCFH-DA staining, Fluo-4-AM staining, JC-1 staining and western blotting were used to determine the changes in cell viability, intracellular reactive oxygen species concentration, Ca 2+ influx, mitochondrial membrane potential and the protein expressions of B-cell lymphoma-2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL). Morphological analysis demonstrated the effect of 5zous on neuritogenesis and differentiation in PC12 cells. The results suggested that 5zou rescued the cell viability, intracellular ROS level, Ca 2+ influx, mitochondrial membrane potential, and expression of Bcl-2 and Bcl-xL, which were altered by 6-OHDA and L-Glu. The study confirmed that 5zou has neuroprotective effects on neurotoxin-induced differentiated PC12 cells injury, potentially via the mitochondrial apoptosis pathway.

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          Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury.

          Elizabeth Murphy, Charles Steenbergen (2008)
          Mitochondria play an important role in cell death and cardioprotection. During ischemia, when ATP is progressively depleted, ion pumps cannot function resulting in a rise in calcium (Ca(2+)), which further accelerates ATP depletion. The rise in Ca(2+) during ischemia and reperfusion leads to mitochondrial Ca(2+) accumulation, particularly during reperfusion when oxygen is reintroduced. Reintroduction of oxygen allows generation of ATP; however, damage to the electron transport chain results in increased mitochondrial generation of reactive oxygen species (ROS). Mitochondrial Ca(2+) overload and increased ROS can result in opening of the mitochondrial permeability transition pore, which further compromises cellular energetics. The resultant low ATP and altered ion homeostasis result in rupture of the plasma membrane and cell death. Mitochondria have long been proposed as central players in cell death, since the mitochondria are central to synthesis of both ATP and ROS and since mitochondrial and cytosolic Ca(2+) overload are key components of cell death. Many cardioprotective mechanisms converge on the mitochondria to reduce cell death. Reducing Ca(2+) overload and reducing ROS have both been reported to reduce ischemic injury. Preconditioning activates a number of signaling pathways that reduce Ca(2+) overload and reduce activation of the mitochondrial permeability transition pore. The mitochondrial targets of cardioprotective signals are discussed in detail.
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            Mitochondrial generation of free radicals and hypoxic signaling.

            Robert O Poyton, Kerri A. Ball, Pablo R. Castello (2009)
            Most reactive oxygen species (ROS) are generated in cells by the mitochondrial respiratory chain. Mitochondrial ROS production is modulated largely by the rate of electron flow through respiratory chain complexes. Recently, it has become clear that under hypoxic conditions, the mitochondrial respiratory chain also produces nitric oxide (NO), which can generate other reactive nitrogen species (RNS). Although excess ROS and RNS can lead to oxidative and nitrosative stress, moderate to low levels of both function in cellular signaling pathways. Especially important are the roles of these mitochondrially generated free radicals in hypoxic signaling pathways, which have important implications for cancer, inflammation and a variety of other diseases.
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              Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease

              Rachelle Balez, Nicole Steiner, Martin Engel … (2016)
              Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases, yet current therapeutic treatments are inadequate due to a complex disease pathogenesis. The plant polyphenol apigenin has been shown to have anti-inflammatory and neuroprotective properties in a number of cell and animal models; however a comprehensive assessment has not been performed in a human model of AD. Here we have used a human induced pluripotent stem cell (iPSC) model of familial and sporadic AD, in addition to healthy controls, to assess the neuroprotective activity of apigenin. The iPSC-derived AD neurons demonstrated a hyper-excitable calcium signalling phenotype, elevated levels of nitrite, increased cytotoxicity and apoptosis, reduced neurite length and increased susceptibility to inflammatory stress challenge from activated murine microglia, in comparison to control neurons. We identified that apigenin has potent anti-inflammatory properties with the ability to protect neurites and cell viability by promoting a global down-regulation of cytokine and nitric oxide (NO) release in inflammatory cells. In addition, we show that apigenin is able to protect iPSC-derived AD neurons via multiple means by reducing the frequency of spontaneous Ca2+ signals and significantly reducing caspase-3/7 mediated apoptosis. These data demonstrate the broad neuroprotective action of apigenin against AD pathogenesis in a human disease model.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Med Rep
                Journal ID (iso-abbrev): Mol Med Rep
                Title: Molecular Medicine Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1791-2997
                ISSN (Electronic): 1791-3004
                Publication date (Print): August 2017
                Publication date (Electronic): 09 June 2017
                Publication date PMC-release: 09 June 2017
                Volume: 16
                Issue: 2
                Pages: 1133-1138
                Affiliations
                [1 ]Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University, Changchun, Jilin 130118, P.R. China
                [2 ]School of Life Sciences, Jilin University, Changchun, Jilin 130012, P.R. China
                [3 ]Zhuhai College of Jilin University, Jilin University, Zhuhai, Guangdong 519041, P.R. China
                Author notes
                Correspondence to: Professor Yu Li, Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University, 2888 Xincheng Street, Changchun, Jilin 130118, P.R. China, E-mail: yuli966@ 123456126.com
                [*]

                Contributed equally

                Article
                Publisher ID: mmr-16-02-1133
                DOI: 10.3892/mmr.2017.6745
                PMC ID: 5562046
                PubMed ID: 28627694
                SO-VID: e3e6a971-8f02-428c-9181-1c3003e42c37
                Copyright © Copyright: © Wang et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 19 May 2016
                Date accepted : 11 April 2017
                Categories
                Subject: Articles

                Keywords: neuroprotection,6-hydroxydopamine,l-glutamate,mitochondria,synthesis
                Data availability:
                Keywords: neuroprotection, 6-hydroxydopamine, l-glutamate, mitochondria, synthesis

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