Combination Therapy with A1 Receptor Agonist and Vitamin C Improved Working Memory in a Mouse Model of Global Ischemia-Reperfusion
Authors
Abstract:
Introduction: Stroke is one of the most important reasons of death. Hence, trials to prevent or lessen the complications originated by stroke are a goal of public health worldwide. The ischemia-reperfusion causes hypoxia, hypoglycemia and incomplete repel of metabolic waste products and leads to accumulation of free radicals triggering neuronal death. The A1 adenosine receptoras an endogenous ligand of adenosine is known to improve cell resistance to destructive agentsby preventing apoptosis. Vitamin C as a cellular antioxidant is also known as an effective factor to reduce damages initiated by free radicals. We studied the protective effects of A1 receptor agonist in combination with vitamin C against ischemia-reperfusion. Methods: Ischemia was induced by common carotid artery occlusion in bulb-c mice (20-30 gr). Y-Maze was employed to scale the short-term memory and Nissl staining was used to count the cells in hippocampus. Results: We found that concurrent treatment of A1 receptor agonist and vitamin C significantly reduced neuronal death in CA1. The Memory scores were also significantly improved (P<0.05). Discussion: Our data point to the therapeutic effects of CPA/vitamin C co-administration and highlight the beneficial role of A1 adenosine receptor signaling in the context of stroke
similar resources
combination therapy with a1 receptor agonist and vitamin c improved working memory in a mouse model of global ischemia-reperfusion
introduction: stroke is one of the most important reasons of death. hence, trials to prevent or lessen the complications originated by stroke are a goal of public health worldwide. the ischemia-reperfusion causes hypoxia, hypoglycemia and incomplete repel of metabolic waste products and leads to accumulation of free radicals triggering neuronal death. the a1 adenosine receptoras an endogenous l...
full textProtective Effects of Hydrocortisone, Vitamin C and E Alone or in Combination against Renal Ischemia-Reperfusion Injury in Rat
Background: Renal ischemia reperfusion injury may occur in a variety of clinical situations, following a transient drop in total or regional blood flow to the kidney. This study was performed to investigate the protective effects of different antioxidants such as vitamin C, vitamin E, hydrocortisone and combination of these agents against experimental renal ischemia-reperfusion injury....
full textSulfur dioxide reduces hippocampal cells death and improves learning and memory deficits in rat model of transient global ischemia/reperfusion
Objective(s): According to recent the findings, sulfur dioxide (SO2) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO2 exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO2 following global cereb...
full textNeuroprotection by a selective estrogen receptor beta agonist in a mouse model of global ischemia.
The present study employs selective estrogen receptor (ER) agonists to determine whether 17beta-estradiol-induced neuroprotection in global ischemia is receptor mediated and, if so, which subtype of receptor (ERalpha or ERbeta) is predominantly responsible. Halothane-anesthetized female C57Bl/6J mice were ovariectomized, and osmotic minipumps containing ERbeta agonist diarylpropiolnitrile (DPN)...
full textNeuroprotection by a selective estrogen receptor agonist in a mouse model of global ischemia
Carswell, H. V. O., I. M. Macrae, L. Gallagher, E. Harrop, and K. J. Horsburgh. Neuroprotection by a selective estrogen receptor agonist in a mouse model of global ischemia. Am J Physiol Heart Circ Physiol 287: H1501–H1504, 2004. First published May 20, 2004; 10.1152/ajpheart.00227.2004.—The present study employs selective estrogen receptor (ER) agonists to determine whether 17 -estradiolinduce...
full textMy Resources
Journal title
volume 4 issue 2
pages 111- 116
publication date 2013-04
By following a journal you will be notified via email when a new issue of this journal is published.
Hosted on Doprax cloud platform doprax.com
copyright © 2015-2023