30
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Brain ischemia initiates several metabolic events leading to neuronal death. These events mediate large amount of damage that arises after some neurodegenerative disorders as well as transient brain ischemia. Melissa officinalis is considered as a helpful herbal plant in the prevention of various neurological diseases like Alzheimer that is related with oxidative stress.

          Methods

          We examined the effect of Melissa officinalis on hypoxia induced neuronal death in a cortical neuronal culture system as in vitro model and transient hippocampal ischemia as in vivo model. Transient hippocampal ischemia was induced in male rats by tow vessel-occlusion for 20 min. After reperfusion, the histopathological changes and the levels inflammation, oxidative stress status, and caspase-3 activity in hippocampus were measured.

          Results

          Cytotoxicity assays showed a significant protection of a 10 μg/ml dose of Melissa against hypoxia in cultured neurons which was confirmed by a conventional staining (P<0.05). Melissa treatment decrease caspase3 activity (P<0.05) and TUNEL-positive cells significantly (P<0.01). Melissa oil has also inhibited malon dialdehyde level and attenuated decrease of Antioxidant Capacity in the hippocampus. Pro-inflammatory cytokines TNF-α, IL-1β and HIF-1α mRNA levels were highly increased after ischemia and treatment with Melissa significantly suppressed HIF-1α gene expression (P<0.05).

          Discussion

          Results showed that Melissa officinalis could be considered as a protective agent in various neurological diseases associated with ischemic brain injury.

          Related collections

          Most cited references31

          • Record: found
          • Abstract: found
          • Article: not found

          A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates.

          1. A new method has been developed for measuring the total antioxidant capacity of body fluids and drug solutions, based on the absorbance of the ABTS.+ radical cation. 2. An automated method for use on a centrifugal analyser, as well as a manual method, is described. 3. The procedure has been applied to physiological antioxidant compounds and radical-scavenging drugs, and an antioxidant ranking was established based on their reactivity relative to a 1.0 mmol/l Trolox standard. 4. The Trolox equivalent antioxidant capacity of plasma from an adult reference population has been measured, and the method optimized and validated. 5. The method has been applied to investigate the total plasma antioxidant capacity of neonates and how this may be compromised in prematurity.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Inflammation in stroke and focal cerebral ischemia.

            A growing number of recent investigations have established a critical role for leukocytes in propagating tissue damage after ischemia and reperfusion in stroke. Experimental data obtained from animal models of middle cerebral artery occlusion implicate inflammatory cell adhesion molecules, chemokines, and cytokines in the pathogenesis of this ischemic damage. Data from recent animal and human studies were reviewed to demonstrate that inflammatory events occurring at the blood-endothelium interface of the cerebral capillaries underlie the resultant ischemic tissue damage. After arterial occlusion, the up-regulated expression of cytokines including IL-1, and IL-6 act upon the vascular endothelium to increase the expression of intercellular adhesion molecule-1, P-selectin, and E-selectin, which promote leukocyte adherence and accumulation. Integrins then serve to structurally modify the basal lamina and extracellular matrix. These inflammatory signals then promote leukocyte transmigration across the endothelium and mediate inflammatory cascades leading to further cerebral infarction. Inflammatory interactions that occur at the blood-endothelium interface, involving cytokines, adhesion molecules, chemokines and leukocytes, are critical to the pathogenesis of tissue damage in cerebral infarction. Exploring these pathophysiological mechanisms underlying ischemic tissue damage may direct rational drug design in the therapeutic treatment of stroke.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Catechin polyphenols: neurodegeneration and neuroprotection in neurodegenerative diseases.

              Neurodegeneration in Parkinson's, Alzheimer's, and other neurodegenerative diseases seems to be multifactorial, in that a complex set of toxic reactions including inflammation, glutamatergic neurotoxicity, increases in iron and nitric oxide, depletion of endogenous antioxidants, reduced expression of trophic factors, dysfunction of the ubiquitin-proteasome system, and expression of proapoptotic proteins leads to the demise of neurons. Thus, the fundamental objective in neurodegeneration and neuroprotection research is to determine which of these factors constitutes the primary event, the sequence in which these events occur, and whether they act in concurrence in the pathogenic process. This has led to the current notion that drugs directed against a single target will be ineffective and rather a single drug or cocktail of drugs with pluripharmacological properties may be more suitable. Green tea catechin polyphenols, formerly thought to be simple radical scavengers, are now considered to invoke a spectrum of cellular mechanisms of action related to their neuroprotective activity. These include pharmacological activities like iron chelation, scavenging of radicals, activation of survival genes and cell signaling pathways, and regulation of mitochondrial function and possibly of the ubiquitin-proteasome system. As a consequence these compounds are receiving significant attention as therapeutic cytoprotective agents for the treatment of neurodegenerative and other diseases.
                Bookmark

                Author and article information

                Journal
                Daru
                Daru
                DARU Journal of Pharmaceutical Sciences
                BioMed Central
                1560-8115
                2008-2231
                2012
                3 October 2012
                : 20
                : 1
                : 42
                Affiliations
                [1 ]Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
                [2 ]Anatomical Sciences Research Center, Kashan University of Medical Sciences, Kashan, Iran
                [3 ]Department of Toxicology - Pharmacology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
                [4 ]Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
                [5 ]Department of Pharmacognosy, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
                [6 ]Department of Neuroscience, School of Advanced Medical Technology, Tehran University of Medical Sciences, Tehran, Iran
                Article
                2008-2231-20-42
                10.1186/2008-2231-20-42
                3555743
                23351182
                87aed26b-eb71-4bb1-bec6-b985c74fad26
                Copyright ©2012 Bayat et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 July 2012
                : 26 September 2012
                Categories
                Research Article

                Pharmacology & Pharmaceutical medicine
                neuron,ischemia,cell death,melissa officinalis,hippocampus
                Pharmacology & Pharmaceutical medicine
                neuron, ischemia, cell death, melissa officinalis, hippocampus

                Comments

                Comment on this article