@2024 Afarand., IRAN
ISSN: 2252-0805 The Horizon of Medical Sciences 2014;20(1):23-27
ISSN: 2252-0805 The Horizon of Medical Sciences 2014;20(1):23-27
Effect of Gallic Acid on Passive Avoidance Memory under Brain Ischemia Conditions in Mature Female Rats
ARTICLE INFO
Article Type
Original ResearchAuthors
Rahimi Asl F. (1 )Farbood Y. (2 )
Sarkaki A.R. (2 )
Hosseini S.E. (* )
(* ) Biology Department, Science Faculty, Fars Science & Research Branch, Islamic Azad University, Marvdasht, Iran
(1 ) Biology Department, Science Faculty, Fars Science & Research Branch, Islamic Azad University, Marvdasht, Iran
(2 ) “Physiology Research Center” & “Physiology Department, Medicine Faculty”, Ahwaz Jundishapur University of Medical Sciences, Ahwaz, Iran
Correspondence
Address: Fars Sciences & Researches Branch, Islamic Azad University, 18th Kilometer of Marvdasht- Sadde Doroodzan Road, Fars, IranPhone: +987284692130
Fax: +987284692110
ebrahim.hossini@yahoo.com
Article History
Received: October 5, 2013Accepted: November 29, 2013
ePublished: February 1, 2014
BRIEF TEXT
From various areas of the brain, Hippocampus area has a very important role concerning memory, learning and fixing any kind of memory [1, 2, 3]. Brain ischemia disrupts brain’s activity and makes an increase in brain oxidants in the lipid peroxidation process [4, 5]. By trapping free radicals, antioxidants cause the body to detoxify [9]. Flavonoid compounds, including Gallic acid, are of powerful antioxidants [10].
Brain ischemia results in severe loss of memory [11]; and oxidative stresses cause inflammatory reactions [12], while Gallic acid prevents these reactions [13]. Gallic acid has antioxidant effect [14].
The aim of this study was to assess the effect of Gallic acid on level of passive avoidance memory among mature female rats, under brain’s bilateral ischemic conditions.
Method of the study is experimental.
Research society was the population of mature female rats with mean weight 200 gr to 250 gr (Animal Reproduction and Breeding Center, Ahwaz University of Medical Sciences, Iran). The study was conducted in Islamic Azad University, Fars Science and Research Branch.
84 mature female rats were studied. The animals were under 12 hour darkness, 12 hour light, and temperature20-22℃ conditions; they were fed with compressed food and water (Pars Tehran, Iran). The rats were randomly divided into 6 groups of 14, as follows: Control (C; without any manipulation of carotid artery and treatment) Gallic Acid Control (CGA; without any manipulation of carotid artery and with Gallic acid treatment) Ischemia Control (CI; with manipulation of carotid artery, but without obstruction and without treatment) Ischemia (I; complete and bilateral obstruction of carotid arteries and without treatment) Solvent Ischemia (IS; complete and bilateral obstruction of carotid arteries under normal saline gavage) Gallic Acid Ischemia (IGA; complete and bilateral obstruction of carotid arteries under Gallic acid gavage) For ischemia conditions, after 8 hours of food deprivation, the animals were anesthetized. Then, creating a gap in the ventral neck and removing adipose tissue and thyroid, carotid arteries were obstructed by means of skin suture instruments and with tight knot around vessels. All prescriptions were applied for 10 days, and after that avoidance memory test was performed. To habituate, the animals were placed in the light part behind the guillotine door, and after 30 seconds with animal’s head turning towards the door, the guillotine door was slowly opened allowing the animal to enter the dark part. Immediately after that, the door was closed. Then, the animal was taken from the dark part and it was transferred into a cage. This step was repeated in 3 stages, after 30 minutes. 30 minutes after adaptation session, learning acquisition was conducted. The animals were placed in the light part. After 30 seconds, the guillotine door was opened. The animal entering the dark part, the door was closed and one mA shock was applied in the animal’s feet for 5 seconds with 50 Hz frequency. Then, allowing the animal to exit from the dark place, after 30 seconds it was taken from the light part and it was returned to the cage. After 2 minutes, if the animal’s behavior was as its own behavior before the experiment and there was no entrance into the dark part for 2 seconds, successful acquisition was registered. Nevertheless, if this was not so, the door was closed and the animal received a shock for second time. 24 hours, 72 hours, and 7 days after training, the rats were tested for retrieval test; in this manner that at first the animals were put in the light part, and after 30 seconds, the guillotine door being opened, time latency before the first entrance into the dark part (Strep-Through Latency; STL) was measured and registered for various groups. Higher STL showed a stronger memory.
To assess passive avoidance learning behavior, Shuttle Box device (Kimia Kahroba-ye-mobin; Iran) was used. The device is composed of “training box” and “control box”. Data were analyzed, by the use of One-way Variance Analysis test (in order to assess differences between groups), LSD Support test (in order to compare each pair of groups), and SPSS 18 software.
24 hours, 72 hours, and 7 days after applying electrical shock, STL time for each of the groups I and IS had a significant decrease than CI group. 24 hours, 72 hours, and 7 days after applying electrical shock, STL time for IGA group had a significant increase than group I. 72 hours after applying electrical shock, STL time for CGA group had a significant increase than CI group. 7 days after applying electrical shock, STL time for IGA group had a significant decrease than CI group.
Non-declared
Non-declared
Non-declared
Gallic acid results in increasing passive avoidance memory in rats with brain ischemia.
The researchers feel grateful to Research Deputy of Islamic Azad University, Fars Science and Research Branch, and officials of Research Center of Ahwaz University of Medical Sciences.
Non-declared
The research’s protocol was prepared according to international laws for care of laboratory animals; and ethic committee of the university approved it.
Non-declared
TABLES and CHARTS
Show attach fileCITIATION LINKS
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[19]Charradi K, Elkahoui S, Karkouch I, Limam F, Hassine FB, Aouani E. Grape seed and skin extract prevents high-fat diet-induced brain lipotoxicity in rat. Neurochem Res. 2012;37(9):2004-12.
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[21]Sarkaki A, Raffiei Rad M, Hoseini SE, Farbood Y, Motamedi F, Mansouri SMT, et al. Improvement in memory and brain long-term potentiation deficits due to permanent Hypoperfusion/Ischemia by Grape Seed Extract in Rats. Iranian J Basic Med Sci. 2013;16:1004-10.
[22] Tung YT, Wu JH, Huang CC, Peng HC, Chen YL, Yang SC, et al. Protective effect of Acacia confusa bark extract and its active compound gallic acid against carbon tetrachloride-induced chronic liver injury in rats. Food Chem Toxicol. 2009;47(6):1385-92.
[23]Lu Z, Nie G, Belton PS, Tang H, Zhao B. Structureactivity relationship analysis of antioxidant ability and neuroprotective effect of gallic acid derivatives. Neurochemistry International. 2006;48(4):263-274.
[24]Stanely Mainzen Prince P, Priscilla H, Devika PT. Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats. Eur J Pharmacol. 2009;615(1):139-43.
[25]Barone FC, Feuerstein GZ. Inflammatory mediators and stroke: new opportunities for novel therapeutics. J Cereb Blood Flow Metab. 2002;19(8):819-834.
[26]Romera C, Hurtado O, Botella S, Lizasoain I, Cardenas A, Fernandez-Tome P, Leza J, Lorenzo P, Moro M. In Vitro Ischemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor- α Pathway. J Neurosci. 2004;24(6):1350- 57.
[27]Liu J, Ginis I, Spatz M, Hallenbeck JM. Hypoxic preconditioning protects cultured neurons against hypoxic stress via TNF-α and ceramide. Am J Physiol Cell Physiol. 2000;278(1):144-53.
[28]Okado-Matsumoto A, Fridovich I. Subcellular dliver istribution of superoxide dismutases (SOD) in rat. J Biol Chem. 2001;276(42):38388-93.
[29]Lee H, Bae JH, Lee SR. Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils. J Neurosci Res. 2004;77(6):892-900.
[2] Mattson MP, Culmsee C, Yu Z, Camandola S. Roles of nuclear factor kappa B in neuronal survival and lasticity. J Neurochem. 2000;74(2):443-56.
[3]Gertner MJ, Thomas SA. The roles of norepinephrine in spatial reference and spatial working memory. CUREJ; 2006.
[4]Hadjinikolaou L, Kotidis K, Galinanes M. Relationship between reduced elasticity of extracardiac vesselsand left main stem coronary artery disease. Eur Heart J. 2004;25(6):508–13.
[5]Raffiei Rad M, Sarkaki A, Hoseini E, Farbood Y, Mansouri SMT, Motamedi F. The effect of Grape Seed Extract Lipid peroxidation duo to ishcemia hypoperfusion in male rat striatum. J Animal Biol. 2011;3(4):37-44.
[6]Endres M, Dirnagl U. Ischemia and stroke. Springer: US; (2002). P. 455-473.
[7]Fisher M. The ischemic penumbra-identification evolution and treatment concepts. Cerebrovasc Dis. 2003;17(supp 1):1-6.
[8] Carr DB, Sesack SR. Projections from the rat prefrontal cortex to the ventral tegmental area: target specificity in the synaptic associations with mesoaccumbens and mesocortical neurons. J Neurosci. 2000;20(10):3864-73.
[9]Kumaran A, Karunakaran RJ. Antioxidant and free radical scavenging activity of an aqueous extract of Coleus aromaticus. Food Chemistry. 2006;97(1):109-14.
[10] Jadon A, Bhadauria M, Shukla S. Protective effect of Terminalia belerica Roxb and gallic acid against carbon tetrachloride induced damage in albino rats. J Ethnopharmacol. 2007;109(2):214-218.
[11]Sarkaki A, Raffiei Rad M, Hoseini SE, Farbood Y, Mansouri SMT, Motamedi F. Cognitive deficiency induced by cerebral hypoperfusion/ischemia improves by exercise and grape seed extact. HealthMed. 2012;6(4):1097-1104.
[12]Mustafa O, Muzaffer K, Resul Y, Erhan K, Fikret O. Free oxygen radical with growth in coelic disease. Health Med. 2011;5(5):1008-13.
[13]Priscilla DH, Prince PSM. Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats. Chemico-Biological Interactions. 2009;179(2):118-24.
[14]Locatelli C, Leal PC, Yunes RA, Nunes RJ, CreczynskiPasa TB. Gallic acid ester derivatives induce apoptosis and cell adhesion inhibition in melanoma cells: the relationship between free radical generation, glutathione depletion and cell death. Chemico-Biological Interactions. 2009;181(2):175-84.
[15]Doyle KP, Simon RP, Stenzel-poore MP. Mechanism of ischemic brain damage. Neuropharmacol. 2008;55(3):310- 18.
[16] Li LX, Cheng YF, Lin HB, Wang C, Xu JP, Zhang HT. Prevention of cerebral Ischemia-induced memory deficit by inhibition of phosphodiesterase-4 in rats. Metab Brain Dis. 2011;26(1):37-47.
[17]Huang L, Chen N, Ge M, Zhu Y, Guan S. Wang JH. Ca2+ and acidosis synergistically lead to the dysfunction of cortical GABAergic neurons during ischemia. Biochem Biophys Res Commun. 2010;394(3):709-14.
[18]Rezayof A, Zare-Chahoki A, Zarrindast MR, Rassouli Y. Inhibition of dorsal hippocampal nitric oxide synthesis potentiates ethanol-induced state-dependent memory in mice. Behav Brain Res. 2010;209(2):189-95.
[19]Charradi K, Elkahoui S, Karkouch I, Limam F, Hassine FB, Aouani E. Grape seed and skin extract prevents high-fat diet-induced brain lipotoxicity in rat. Neurochem Res. 2012;37(9):2004-12.
[20]Liu P, Smith PF, Appleton I, Darlington CL, Bilkey DK. Regional variations and age-related changes in nitric oxide synthase and arginase in the sub-egions of the hippocampus. Neuroscience. 2003;119(3):679-87.
[21]Sarkaki A, Raffiei Rad M, Hoseini SE, Farbood Y, Motamedi F, Mansouri SMT, et al. Improvement in memory and brain long-term potentiation deficits due to permanent Hypoperfusion/Ischemia by Grape Seed Extract in Rats. Iranian J Basic Med Sci. 2013;16:1004-10.
[22] Tung YT, Wu JH, Huang CC, Peng HC, Chen YL, Yang SC, et al. Protective effect of Acacia confusa bark extract and its active compound gallic acid against carbon tetrachloride-induced chronic liver injury in rats. Food Chem Toxicol. 2009;47(6):1385-92.
[23]Lu Z, Nie G, Belton PS, Tang H, Zhao B. Structureactivity relationship analysis of antioxidant ability and neuroprotective effect of gallic acid derivatives. Neurochemistry International. 2006;48(4):263-274.
[24]Stanely Mainzen Prince P, Priscilla H, Devika PT. Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats. Eur J Pharmacol. 2009;615(1):139-43.
[25]Barone FC, Feuerstein GZ. Inflammatory mediators and stroke: new opportunities for novel therapeutics. J Cereb Blood Flow Metab. 2002;19(8):819-834.
[26]Romera C, Hurtado O, Botella S, Lizasoain I, Cardenas A, Fernandez-Tome P, Leza J, Lorenzo P, Moro M. In Vitro Ischemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor- α Pathway. J Neurosci. 2004;24(6):1350- 57.
[27]Liu J, Ginis I, Spatz M, Hallenbeck JM. Hypoxic preconditioning protects cultured neurons against hypoxic stress via TNF-α and ceramide. Am J Physiol Cell Physiol. 2000;278(1):144-53.
[28]Okado-Matsumoto A, Fridovich I. Subcellular dliver istribution of superoxide dismutases (SOD) in rat. J Biol Chem. 2001;276(42):38388-93.
[29]Lee H, Bae JH, Lee SR. Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils. J Neurosci Res. 2004;77(6):892-900.