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CORM-3, a carbon monoxide-releasing molecule, alters the inflammatory response and reduces brain damage in a rat model of hemorrhagic stroke. / Yabluchanskiy, Andriy; Sawle, Philip; Homer-Vanniasinkam, Shervanthi; Green, Colin J; Foresti, Roberta; Motterlini, Roberto.

In: Critical Care Medicine, Vol. 40, No. 2, 02.2012, p. 544-52.

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Yabluchanskiy, Andriy ; Sawle, Philip ; Homer-Vanniasinkam, Shervanthi ; Green, Colin J ; Foresti, Roberta ; Motterlini, Roberto. / CORM-3, a carbon monoxide-releasing molecule, alters the inflammatory response and reduces brain damage in a rat model of hemorrhagic stroke. In: Critical Care Medicine. 2012 ; Vol. 40, No. 2. pp. 544-52.

Bibtex

@article{706173d60e0643189ada074823271206,
title = "CORM-3, a carbon monoxide-releasing molecule, alters the inflammatory response and reduces brain damage in a rat model of hemorrhagic stroke",
abstract = "OBJECTIVE: Intracerebral hemorrhage is accompanied by a pronounced inflammatory response that mediates brain damage but is also essential for the tissue reparative process. We assessed the effect of CORM-3, a water-soluble carbon monoxide-releasing molecule possessing anti-inflammatory properties, on inflammation and brain injury after intracerebral hemorrhage.DESIGN: In vivo and in vitro laboratory study.SETTING: Research laboratory.SUBJECTS: Male Sprague-Dawley rats, 250-350 g.INTERVENTIONS: A model of collagenase injection (2 μL) in the brain was established to induce intracerebral hemorrhage. CORM-3 (4 or 8 mg/kg) was administered intravenously at different times as follows: 1) 5 mins before collagenase; 2) 3 hrs after collagenase; and 3) 3 days after collagenase challenge.MEASUREMENTS AND MAIN RESULTS: Saline was used as a negative control. Brain damage, brain water content, and behavioral assessment were evaluated. The inflammatory response was determined at set intervals after intracerebral hemorrhage by counting peripheral neutrophils and lymphocytes, neutrophils, and activated microglia/macrophages in the intracerebral hemorrhage area and measuring plasma tumor necrosis factor-{\'a} levels. BV2 microglia and DI-TNC1 astrocytes were exposed to triton (1%) or CORM-3 (10-100 {\`i}M) and cytotoxicity (lactic dehydrogenase assay) measured at 24 hrs. A challenge with collagenase to induce intracerebral hemorrhage caused marked brain damage and modified the levels of inflammatory markers. Pretreatment with CORM-3 significantly prevented injury, modulated inflammation, and reduced plasma tumor necrosis factor-α. CORM-3 given 3 hrs after collagenase significantly increased brain injury and tumor necrosis factor-α production. In contrast, CORM-3 given 3 days after collagenase afforded partial protection, modulated inflammation, and decreased tumor necrosis factor-α starting from the day of application. No dose-dependent effects were observed.CONCLUSIONS: CORM-3 promotes neuroprotection or neurotoxicity after intracerebral hemorrhage depending on the time of administration. Beneficial effects are achieved when CORM-3 is given either before or 3 days after intracerebral hemorrhage, namely, as a prophylactic agent or during the postacute inflammatory phase.",
keywords = "Animals, Brain Injuries, Cerebral Hemorrhage, Disease Models, Animal, Immunohistochemistry, Inflammation, Inflammation Mediators, Male, Neuroprotective Agents, Organometallic Compounds, Random Allocation, Rats, Rats, Sprague-Dawley, Reference Values, Risk Assessment, Severity of Illness Index, Survival Rate, Treatment Outcome, Tumor Necrosis Factor-alpha, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't",
author = "Andriy Yabluchanskiy and Philip Sawle and Shervanthi Homer-Vanniasinkam and Green, {Colin J} and Roberta Foresti and Roberto Motterlini",
year = "2012",
month = feb,
doi = "10.1097/CCM.0b013e31822f0d64",
language = "English",
volume = "40",
pages = "544--52",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins Ltd.",
number = "2",

}

RIS

TY - JOUR

T1 - CORM-3, a carbon monoxide-releasing molecule, alters the inflammatory response and reduces brain damage in a rat model of hemorrhagic stroke

AU - Yabluchanskiy, Andriy

AU - Sawle, Philip

AU - Homer-Vanniasinkam, Shervanthi

AU - Green, Colin J

AU - Foresti, Roberta

AU - Motterlini, Roberto

PY - 2012/2

Y1 - 2012/2

N2 - OBJECTIVE: Intracerebral hemorrhage is accompanied by a pronounced inflammatory response that mediates brain damage but is also essential for the tissue reparative process. We assessed the effect of CORM-3, a water-soluble carbon monoxide-releasing molecule possessing anti-inflammatory properties, on inflammation and brain injury after intracerebral hemorrhage.DESIGN: In vivo and in vitro laboratory study.SETTING: Research laboratory.SUBJECTS: Male Sprague-Dawley rats, 250-350 g.INTERVENTIONS: A model of collagenase injection (2 μL) in the brain was established to induce intracerebral hemorrhage. CORM-3 (4 or 8 mg/kg) was administered intravenously at different times as follows: 1) 5 mins before collagenase; 2) 3 hrs after collagenase; and 3) 3 days after collagenase challenge.MEASUREMENTS AND MAIN RESULTS: Saline was used as a negative control. Brain damage, brain water content, and behavioral assessment were evaluated. The inflammatory response was determined at set intervals after intracerebral hemorrhage by counting peripheral neutrophils and lymphocytes, neutrophils, and activated microglia/macrophages in the intracerebral hemorrhage area and measuring plasma tumor necrosis factor-á levels. BV2 microglia and DI-TNC1 astrocytes were exposed to triton (1%) or CORM-3 (10-100 ìM) and cytotoxicity (lactic dehydrogenase assay) measured at 24 hrs. A challenge with collagenase to induce intracerebral hemorrhage caused marked brain damage and modified the levels of inflammatory markers. Pretreatment with CORM-3 significantly prevented injury, modulated inflammation, and reduced plasma tumor necrosis factor-α. CORM-3 given 3 hrs after collagenase significantly increased brain injury and tumor necrosis factor-α production. In contrast, CORM-3 given 3 days after collagenase afforded partial protection, modulated inflammation, and decreased tumor necrosis factor-α starting from the day of application. No dose-dependent effects were observed.CONCLUSIONS: CORM-3 promotes neuroprotection or neurotoxicity after intracerebral hemorrhage depending on the time of administration. Beneficial effects are achieved when CORM-3 is given either before or 3 days after intracerebral hemorrhage, namely, as a prophylactic agent or during the postacute inflammatory phase.

AB - OBJECTIVE: Intracerebral hemorrhage is accompanied by a pronounced inflammatory response that mediates brain damage but is also essential for the tissue reparative process. We assessed the effect of CORM-3, a water-soluble carbon monoxide-releasing molecule possessing anti-inflammatory properties, on inflammation and brain injury after intracerebral hemorrhage.DESIGN: In vivo and in vitro laboratory study.SETTING: Research laboratory.SUBJECTS: Male Sprague-Dawley rats, 250-350 g.INTERVENTIONS: A model of collagenase injection (2 μL) in the brain was established to induce intracerebral hemorrhage. CORM-3 (4 or 8 mg/kg) was administered intravenously at different times as follows: 1) 5 mins before collagenase; 2) 3 hrs after collagenase; and 3) 3 days after collagenase challenge.MEASUREMENTS AND MAIN RESULTS: Saline was used as a negative control. Brain damage, brain water content, and behavioral assessment were evaluated. The inflammatory response was determined at set intervals after intracerebral hemorrhage by counting peripheral neutrophils and lymphocytes, neutrophils, and activated microglia/macrophages in the intracerebral hemorrhage area and measuring plasma tumor necrosis factor-á levels. BV2 microglia and DI-TNC1 astrocytes were exposed to triton (1%) or CORM-3 (10-100 ìM) and cytotoxicity (lactic dehydrogenase assay) measured at 24 hrs. A challenge with collagenase to induce intracerebral hemorrhage caused marked brain damage and modified the levels of inflammatory markers. Pretreatment with CORM-3 significantly prevented injury, modulated inflammation, and reduced plasma tumor necrosis factor-α. CORM-3 given 3 hrs after collagenase significantly increased brain injury and tumor necrosis factor-α production. In contrast, CORM-3 given 3 days after collagenase afforded partial protection, modulated inflammation, and decreased tumor necrosis factor-α starting from the day of application. No dose-dependent effects were observed.CONCLUSIONS: CORM-3 promotes neuroprotection or neurotoxicity after intracerebral hemorrhage depending on the time of administration. Beneficial effects are achieved when CORM-3 is given either before or 3 days after intracerebral hemorrhage, namely, as a prophylactic agent or during the postacute inflammatory phase.

KW - Animals

KW - Brain Injuries

KW - Cerebral Hemorrhage

KW - Disease Models, Animal

KW - Immunohistochemistry

KW - Inflammation

KW - Inflammation Mediators

KW - Male

KW - Neuroprotective Agents

KW - Organometallic Compounds

KW - Random Allocation

KW - Rats

KW - Rats, Sprague-Dawley

KW - Reference Values

KW - Risk Assessment

KW - Severity of Illness Index

KW - Survival Rate

KW - Treatment Outcome

KW - Tumor Necrosis Factor-alpha

KW - Comparative Study

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1097/CCM.0b013e31822f0d64

DO - 10.1097/CCM.0b013e31822f0d64

M3 - Article

C2 - 21926571

VL - 40

SP - 544

EP - 552

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 2

ER -