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      Tea polyphenols increase X-ray repair cross-complementing protein 1 and apurinic/apyrimidinic endonuclease/redox factor-1 expression in the hippocampus of rats during cerebral ischemia/reperfusion injury★

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          Abstract

          Recent studies have shown that tea polyphenols can cross the blood-brain barrier, inhibit apoptosis and play a neuroprotective role against cerebral ischemia. Furthermore, tea polyphenols can decrease DNA damage caused by free radicals. We hypothesized that tea polyphenols repair DNA damage and inhibit neuronal apoptosis during global cerebral ischemia/reperfusion. To test this hypothesis, we employed a rat model of global cerebral ischemia/reperfusion. We demonstrated that intraperitoneal injection of tea polyphenols immediately after reperfusion significantly reduced apoptosis in the hippocampal CA1 region; this effect started 6 hours following reperfusion. Immunohistochemical staining showed that tea polyphenols could reverse the ischemia/reperfusion-induced reduction in the expression of DNA repair proteins, X-ray repair cross-complementing protein 1 and apurinic/apyrimidinic endonuclease/redox factor-1 starting at 2 hours. Both effects lasted at least 72 hours. These experimental findings suggest that tea polyphenols promote DNA damage repair and protect against apoptosis in the brain.

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          Apoptosis-inducing factor mediates poly(ADP-ribose) (PAR) polymer-induced cell death.

          Guy Poirier, Shaida A. Andrabi, Hongmin Wang … (2006)
          Apoptosis-inducing factor (AIF), a mitochondrial oxidoreductase, is released into the cytoplasm to induce cell death in response to poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) activation. How PARP-1 activation leads to AIF release is not known. Here we identify PAR polymer as a cell death signal that induces release of AIF. PAR polymer induces mitochondrial AIF release and translocation to the nucleus. PAR glycohydrolase, which degrades PAR polymer, prevents PARP-1-dependent AIF release. Cells with reduced levels of AIF are resistant to PARP-1-dependent cell death and PAR polymer cytotoxicity. These results reveal PAR polymer as an AIF-releasing factor that plays important roles in PARP-1-dependent cell death.
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            Role of oxidants in ischemic brain damage.

            Paul K S Chan (1996)
            Oxygen free radicals or oxidants have been proposed to be involved in acute central nervous system injury that is produced by cerebral ischemia and reperfusion. Because of the transient nature of oxygen radicals and the technical difficulties inherent in accurately measuring their levels in the brain, experimental strategies have been focused on the use of pharmacological agents and antioxidants to seek a correlation between the exogenously supplied specific radical scavengers (ie, superoxide dismutase and catalase) and the subsequent protection of cerebral tissues from ischemic injury. However, this strategy entails problems (hemodynamic, pharmacokinetic, toxicity, blood-brain barrier permeability, etc) that may cloud the data interpretation. This mini-review will focus on the oxidant mechanisms in cerebral ischemic brain injury by using transgenic and knockout mice as an alternative approach. Transgenic and knockout mutants that either overexpress or are deficient in antioxidant enzyme/protein levels have been successfully produced. The availability of these genetically modified animals has made it possible to investigate the role of certain oxidants in ischemic brain cell damage in molecular fashion. It has been shown that an increased level of CuZn-superoxide dismutase and antiapoptotic protein Bcl-2 in the brains of transgenic mice protects neurons from ischemic/reperfusion injury, whereas a deficiency in CuZn-superoxide dismutase or mitochondrial Mn-superoxide dismutase exacerbates ischemic brain damage. Target disruption of neuronal nitric oxide synthase in mice also provides neuronal protection against permanent and transient focal cerebral ischemia. I conclude that molecular genetic approaches in modifying antioxidant levels in the brain offer a unique tool for understanding the role of oxidants in ischemic brain damage.
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              XRCC1 coordinates the initial and late stages of DNA abasic site repair through protein-protein interactions.

              A E Vidal, S. Boiteux, I D Hickson … (2001)
              The major human AP endonuclease APE1 (HAP1, APEX, Ref1) initiates the repair of abasic sites generated either spontaneously, from attack of bases by free radicals, or during the course of the repair of damaged bases. APE1 therefore plays a central role in the base excision repair (BER) pathway. We report here that XRCC1, another essential protein involved in the maintenance of genome stability, physically interacts with APE1 and stimulates its enzymatic activities. A truncated form of APE1, lacking the first 35 amino acids, although catalytically proficient, loses the affinity for XRCC1 and is not stimulated by XRCC1. Chinese ovary cell lines mutated in XRCC1 have a diminished capacity to initiate the repair of AP sites. This defect is compensated by the expression of XRCC1. XRCC1, acting as both a scaffold and a modulator of the different activities involved in BER, would provide a physical link between the incision and sealing steps of the AP site repair process. The interaction described extends the coordinating role of XRCC1 to the initial step of the repair of DNA abasic sites.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Regen Res
                Journal ID (iso-abbrev): Neural Regen Res
                Journal ID (publisher-id): NRR
                Title: Neural Regeneration Research
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 1673-5374
                ISSN (Electronic): 1876-7958
                Publication date (Print): 25 October 2012
                Volume: 7
                Issue: 30
                Pages: 2355-2361
                Affiliations
                [1 ] Department of Anesthesiology, Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China
                [2 ] Department of Anesthesiology, Stomatological Hospital, Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China
                Author notes
                [★]

                Zhi Wang, Master, Attending physician, Department of Anesthesiology, Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China; Department of Anesthesiology, Stomatological Hospital, Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China

                Corresponding author: Rongliang Xue, Professor, Department of Anesthesiology, Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China wz9602@ 123456sina.com . (N20120107001/H)

                Author contributions: Rongliang Xue was responsible for funding, designed this study and revised the manuscript. Zhi Wang provided experimental data, participated in statistical analysis and wrote the manuscript. Xi Lei and Jianrui Lv revised the first version of the manuscript. Gang Wu and Wei Li provided technical support and performed statistical calculations. Li Xue and Xiaoming Lei provided information support. Hongxia Zhao, Hui Gao and Xin Wei participated in experimental animal breeding and processing.

                Article
                Publisher ID: NRR-7-2355
                DOI: 10.3969/j.issn.1673-5374.2012.30.005
                PMC ID: 4268741
                SO-VID: a5ece819-cb1b-45f4-a2e9-acd48a00eda1
                Copyright © Copyright: © Neural Regeneration Research
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 20 April 2012
                Date accepted : 22 August 2012
                Categories
                Subject: Research and Report: Traditional Chinese Medicine and Neural Regeneration

                Keywords: global cerebral ischemia/reperfusion,x-ray repair cross-complementing protein 1,apurinic/apyrimidinic endonuclease/redox factor-1,tea polyphenols
                Data availability:
                Keywords: global cerebral ischemia/reperfusion, x-ray repair cross-complementing protein 1, apurinic/apyrimidinic endonuclease/redox factor-1, tea polyphenols

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