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      • Record: found
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      Antioxidant and Anti-inflammatory Mechanisms of Neuroprotection by Ursolic Acid: Addressing Brain Injury, Cerebral Ischemia, Cognition Deficit, Anxiety, and Depression

      review-article
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      Publication date (Electronic):
      Journal: Oxidative Medicine and Cellular Longevity
      Publisher: Hindawi

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          Abstract

          Ursolic acid (UA) is a pentacyclic triterpene which is found in common herbs and medicinal plants that are reputed for a variety of pharmacological effects. Both as an active principle of these plants and as a nutraceutical ingredient, the pharmacology of UA in the CNS and other organs and systems has been extensively reported in recent years. In this communication, the antioxidant and anti-inflammatory axis of UA's pharmacology is appraised for its therapeutic potential in some common CNS disorders. Classic examples include the traumatic brain injury (TBI), cerebral ischemia, cognition deficit, anxiety, and depression. The pharmacological efficacy for UA is demonstrated through the therapeutic principle of one drug → multitargets → one/many disease(s). Both specific enzymes and receptor targets along with diverse pharmacological effects associated with oxidative stress and inflammatory signalling are scrutinised.

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          The Nrf2-antioxidant response element signaling pathway and its activation by oxidative stress.

          Truyen Nguyen, Paul Nioi, Cecil B. Pickett (2009)
          A major mechanism in the cellular defense against oxidative or electrophilic stress is activation of the Nrf2-antioxidant response element signaling pathway, which controls the expression of genes whose protein products are involved in the detoxication and elimination of reactive oxidants and electrophilic agents through conjugative reactions and by enhancing cellular antioxidant capacity. At the molecular level, however, the regulatory mechanisms involved in mediating Nrf2 activation are not fully understood. It is well established that Nrf2 activity is controlled, in part, by the cytosolic protein Keap1, but the nature of this pathway and the mechanisms by which Keap1 acts to repress Nrf2 activity remain to be fully characterized and are the topics of discussion in this minireview. In addition, a possible role of the Nrf2-antioxidant response element transcriptional pathway in neuroprotection will also be discussed.
          Article 0 comments Cited 817 times – based on 0 reviews     Review now
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            Molecular basis of Klotho: from gene to function in aging.

            Yuechi Xu, Zhongjie Sun (2015)
            The discovery of the Klotho (KL) gene, which was originally identified as a putative aging-suppressor gene, has generated tremendous interest and has advanced understanding of the aging process. In mice, the overexpression of the KL gene extends the life span, whereas mutations to the KL gene shorten the life span. The human KL gene encodes the α-Klotho protein, which is a multifunctional protein that regulates the metabolism of phosphate, calcium, and vitamin D. α-Klotho also may function as a hormone, although the α-Klotho receptor(s) has not been found. Point mutations of the KL gene in humans are associated with hypertension and kidney disease, which suggests that α-Klotho may be essential to the maintenance of normal renal function. Three α-Klotho protein types with potentially different functions have been identified: a full-length transmembrane α-Klotho, a truncated soluble α-Klotho, and a secreted α-Klotho. Recent evidence suggests that α-Klotho suppresses the insulin and Wnt signaling pathways, inhibits oxidative stress, and regulates phosphatase and calcium absorption. In this review, we provide an update on recent advances in the understanding of the molecular, genetic, biochemical, and physiological properties of the KL gene. Specifically, this review focuses on the structure of the KL gene and the factors that regulate KL gene transcription, the key sites in the regulation of α-Klotho enzyme activity, the α-Klotho signaling pathways, and the molecular mechanisms that underlie α-Klotho function. This current understanding of the molecular biology of the α-Klotho protein may offer new insights into its function and role in aging.
            Article 0 comments Cited 173 times – based on 0 reviews     Review now
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              Microglial Activation in Traumatic Brain Injury

              Cornelius K Donat, Gregory Scott, Steve Gentleman … (2017)
              Microglia have a variety of functions in the brain, including synaptic pruning, CNS repair and mediating the immune response against peripheral infection. Microglia rapidly become activated in response to CNS damage. Depending on the nature of the stimulus, microglia can take a number of activation states, which correspond to altered microglia morphology, gene expression and function. It has been reported that early microglia activation following traumatic brain injury (TBI) may contribute to the restoration of homeostasis in the brain. On the other hand, if they remain chronically activated, such cells display a classically activated phenotype, releasing pro-inflammatory molecules, resulting in further tissue damage and contributing potentially to neurodegeneration. However, new evidence suggests that this classification is over-simplistic and the balance of activation states can vary at different points. In this article, we review the role of microglia in TBI, analyzing their distribution, morphology and functional phenotype over time in animal models and in humans. Animal studies have allowed genetic and pharmacological manipulations of microglia activation, in order to define their role. In addition, we describe investigations on the in vivo imaging of microglia using translocator protein (TSPO) PET and autoradiography, showing that microglial activation can occur in regions far remote from sites of focal injuries, in humans and animal models of TBI. Finally, we outline some novel potential therapeutic approaches that prime microglia/macrophages toward the beneficial restorative microglial phenotype after TBI.
              Article 0 comments Cited 163 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Solomon Habtemariam:
                ORCID: http://orcid.org/0000-0001-6743-2244
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2019
                Publication date (Electronic): 16 May 2019
                Volume: 2019
                Electronic Location Identifier: 8512048
                Affiliations
                Pharmacognosy Research Laboratories & Herbal Analysis Services, University of Greenwich, Central Avenue, Chatham-Maritime, Kent ME4 4TB, UK
                Author notes

                Academic Editor: José P. Andrade

                Author information
                http://orcid.org/0000-0001-6743-2244
                Article
                DOI: 10.1155/2019/8512048
                PMC ID: 6541953
                PubMed ID: 31223427
                SO-VID: 954f2193-444e-4c5b-b398-11db6fba3203
                Copyright © Copyright © 2019 Solomon Habtemariam.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 February 2019
                Date revision received : 27 April 2019
                Date accepted : 8 May 2019
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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