ArticleWorld journal of gastroenterology2005
Effect of glutamate on inflammatory responses of intestine and brain after focal cerebral ischemia.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 49 citations in OpenAlex.
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- Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells.Neuroscience bulletin · 2018Article
- Application of nanostructured lipid carriers: the prolonged protective effects for sesamol in in vitro and in vivo models of ischemic stroke via activation of PI3K signalling pathway.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2017Article
- Cinepazide maleate protects PC12 cells against oxygen-glucose deprivation-induced injury.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
- Ketamine and the myenteric plexus in intestinal ischemia/reperfusion injury.Digestive diseases and sciences · 2010Article
- PGF(2alpha) FP receptor contributes to brain damage following transient focal brain ischemia.Neurotoxicity research · 2009Article
- Protein-energy malnutrition increases activation of the transcription factor, nuclear factor kappaB, in the gerbil hippocampus following global ischemia.The Journal of nutritional biochemistry · 2008Article
- Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats.World journal of gastroenterology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the modulation of glutamate on post-ischemic intestinal and cerebral inflammatory responses in a ischemic and excitotoxic rat model.
methodsAdult male rats were subjected to bilateral carotid artery occlusion for 15 min and injection of monosodium glutamate intraperitoneally, to decapitate them at selected time points. Tumor necrosis factor alpha (TNF-alpha) level and nuclear factor kappa B (NF-kappaB) activity were determined by enzyme-linked immunosorbant assay (ELISA) and electrophoretic mobility shift assay (EMSA), respectively. Hemodynamic parameters were monitored continuously during the whole process of cerebral ischemia and reperfusion.
resultsMonosodium glutamate (MSG) treated rats displayed statistically significant high levels of TNF-alpha in cerebral and intestinal tissues within the first 6 h of ischemia. The rats with cerebral ischemia showed a minor decrease of TNF-alpha production in cerebral and intestinal tissues. The rats with cerebral ischemia and treated with MSG displayed statistically significant low levels of TNF-alpha in cerebral and intestinal tissues. These results correlated significantly with NF-kappaB production calculated at the same intervals. During experiment, the mean blood pressure and heart rates in all groups were stable.
conclusionGlutamate is involved in the mechanism of intestinal and cerebral inflammation responses. The effects of glutamate on cerebral and intestinal inflammatory responses after ischemia are up-regulated at the transcriptional level, through the NF-kappaB signal transduction pathway.
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