Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization

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Autore principale: Catalina Lapuente Chala
Natura: Artículo científico
Lingua:en
Pubblicazione: Universidad del Valle 2013
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author Catalina Lapuente Chala
author_facet Catalina Lapuente Chala
contents Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization Catalina Lapuente Chala Carlos Augusto Rengifo Valbuena Marco Fidel Ávila Rodríguez Angela de Céspedes Rubio Medicina astrocytes neuroglia gliosis immunohistochemistry Brain cerebral ischemia dimethyl sulfoxide (DMSO) Introduction: The pathophysiology of cerebral ischemia is essential for early diagnosis, neurologic recovery, the early onset of drug treatment and the prognosis of ischemic events. Experimental models of cerebral ischemia can be used to evaluate the cellular response phenomena and possible neurological protection by drugs. Objective: To characterize the cellular changes in the neuronal population and astrocytic response by the effect of Dimethyl Sulfoxide (DMSO) on a model of ischemia caused by cerebral embolism. Methods: Twenty Wistar rats were divided into four groups (n = 5). The infarct was induced with α-bovine thrombin (40 NIH/Unit.). The treated group received 90 mg (100 ul) of DMSO in saline (1:1 v/v) intraperitoneally for 5 days; ischemic controls received only NaCl (placebo) and two non-ischemic groups (simulated) received NaCl and DMSO respectively. We evaluated the neuronal (anti-NeuN) and astrocytic immune reactivity (anti-GFAP). The results were analyzed by densitometry (NIH Image J-Fiji 1.45 software) and analysis of variance (ANOVA) with the Graph pad software (Prism 5). Results: Cerebral embolism induced reproducible and reliable lesions in the cortex and hippocampus (CA1)., similar to those of focal models. DMSO did not reverse the loss of post-ischemia neuronal immune reactivity, but prevented the morphological damage of neurons, and significantly reduced astrocytic hyperactivity in the somato-sensory cortex and CA1 (P <0.001).Conclusions: The regulatory effect of DMSO on astrocyte hyperreactivity and neuronal-astroglialcytoarchitecture , gives it potential neuroprotective properties for the treatment of thromboembolic cerebral ischemia in the acute phase. 2013 artículo científico 0120-8322 https://www.redalyc.org/articulo.oa?id=28325629006 https://www.redalyc.org/journal/283/28325629006/ https://www.redalyc.org/journal/283/28325629006/html/ https://www.redalyc.org/journal/283/28325629006/28325629006.epub https://www.redalyc.org/journal/283/28325629006/movil en http://www.redalyc.org/revista.oa?id=283 Colombia Médica application/pdf Universidad del Valle Colombia Médica (Colombia) Num.1 Vol.44
format Artículo científico
id redalyc_28325629006
institution Redalyc
language en
publishDate 2013
publisher Universidad del Valle
spellingShingle Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization
Catalina Lapuente Chala
Medicina
astrocytes
neuroglia gliosis
immunohistochemistry
Brain cerebral ischemia
dimethyl sulfoxide (DMSO)
Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization Catalina Lapuente Chala Carlos Augusto Rengifo Valbuena Marco Fidel Ávila Rodríguez Angela de Céspedes Rubio Medicina astrocytes neuroglia gliosis immunohistochemistry Brain cerebral ischemia dimethyl sulfoxide (DMSO) Introduction: The pathophysiology of cerebral ischemia is essential for early diagnosis, neurologic recovery, the early onset of drug treatment and the prognosis of ischemic events. Experimental models of cerebral ischemia can be used to evaluate the cellular response phenomena and possible neurological protection by drugs. Objective: To characterize the cellular changes in the neuronal population and astrocytic response by the effect of Dimethyl Sulfoxide (DMSO) on a model of ischemia caused by cerebral embolism. Methods: Twenty Wistar rats were divided into four groups (n = 5). The infarct was induced with α-bovine thrombin (40 NIH/Unit.). The treated group received 90 mg (100 ul) of DMSO in saline (1:1 v/v) intraperitoneally for 5 days; ischemic controls received only NaCl (placebo) and two non-ischemic groups (simulated) received NaCl and DMSO respectively. We evaluated the neuronal (anti-NeuN) and astrocytic immune reactivity (anti-GFAP). The results were analyzed by densitometry (NIH Image J-Fiji 1.45 software) and analysis of variance (ANOVA) with the Graph pad software (Prism 5). Results: Cerebral embolism induced reproducible and reliable lesions in the cortex and hippocampus (CA1)., similar to those of focal models. DMSO did not reverse the loss of post-ischemia neuronal immune reactivity, but prevented the morphological damage of neurons, and significantly reduced astrocytic hyperactivity in the somato-sensory cortex and CA1 (P <0.001).Conclusions: The regulatory effect of DMSO on astrocyte hyperreactivity and neuronal-astroglialcytoarchitecture , gives it potential neuroprotective properties for the treatment of thromboembolic cerebral ischemia in the acute phase. 2013 artículo científico 0120-8322 https://www.redalyc.org/articulo.oa?id=28325629006 https://www.redalyc.org/journal/283/28325629006/ https://www.redalyc.org/journal/283/28325629006/html/ https://www.redalyc.org/journal/283/28325629006/28325629006.epub https://www.redalyc.org/journal/283/28325629006/movil en http://www.redalyc.org/revista.oa?id=283 Colombia Médica application/pdf Universidad del Valle Colombia Médica (Colombia) Num.1 Vol.44
title Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization
topic Medicina
astrocytes
neuroglia gliosis
immunohistochemistry
Brain cerebral ischemia
dimethyl sulfoxide (DMSO)
url https://www.redalyc.org/articulo.oa?id=28325629006
https://www.redalyc.org/journal/283/28325629006/
https://www.redalyc.org/journal/283/28325629006/html/
https://www.redalyc.org/journal/283/28325629006/28325629006.epub
https://www.redalyc.org/journal/283/28325629006/movil