Contribution of Cerebral Edema to the Neuronal Salvage Elicited by Stimulation of Cerebellar Fastigial Nucleus after Occlusion of the Middle Cerebral Artery in Rat

Golanov, Eugene V.; Reis, Donald J.

doi:10.1038/jcbfm.1995.19

Cited by 67 publications

(40 citation statements)

References 22 publications

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“…Coronal frozen sections of brain (20 mm-thick) were stained using a solution of 1% cresyl violet in 0.25% acetic acid and mounted with Entellan. The striatal and cortical areas of infarction, outlined in light were measured on each section using a computer image analysis system and corrected for brain edema according to Golanov and Reis [30] . Infarct volume, expressed in mm 3 , was calculated by a linear integration of the corrected lesions areas as previously described [24].…”

Section: Measurements Of Infarct Volume Brain Edema and Bbb Leakagementioning

confidence: 99%

MLC901 Favors Angiogenesis and Associated Recovery after Ischemic Stroke in Mice

Gandin

Widmann²,

Lazdunski³

et al. 2016

Cerebrovasc Dis

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Background: There is increasing evidence that angiogenesis, through new blood vessel formation, results in improved collateral circulation and may impact the long-term recovery of patients. In this study, we first investigated the preventive action of a 5-week pretreatment of MLC901, an herbal extract preparation derived from Chinese medicine, against the deleterious effects of ischemic stroke and its effects on angiogenesis in a model of focal ischemia in mice. Methods: The stroke model was induced by 60 min of middle cerebral artery occlusion followed by reperfusion. MLC901 was administered in the drinking water of animals (6 g/l) for 5 weeks before ischemia and then during reperfusion. Results: MLC901 treatment increased the survival rate, reduced the cerebral infarct area and attenuated the blood brain barrier leakage as well as the neurologic dysfunction following ischemia and reperfusion. We provide evidence that MLC901 enhances endothelial cell proliferation and angiogenesis by increasing the number of neocortical vessels in the infarcted area. MLC901 regulates the expression of hypoxic inducible factor 1α and its downstream targets such as vascular endothelial growth factor and angiopoietins 1 and 2. This work also shows that erythropoietin is an important player in the enhancement of angiogenesis by MLC901. Conclusions: These results demonstrate therapeutic properties of MLC901, in addition to those previously described, in stimulating revascularization, neuroprotection and repair of the neurovascular unit after ischemic stroke.

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Section: Measurements Of Infarct Volume Brain Edema and Bbb Leakagementioning

confidence: 99%

MLC901 Favors Angiogenesis and Associated Recovery after Ischemic Stroke in Mice

Gandin

Widmann²,

Lazdunski³

et al. 2016

Cerebrovasc Dis

View full text Add to dashboard Cite

show abstract

“…Coronal frozen sections of brain (20 mm-thick) were stained using a solution of 1% cresyl violet in 0.25% acetic acid, and mounted with Entellan. The striatal and cortical areas of infarction, outlined in light were measured on each section using a computer image analysis system and corrected for brain edema according to Golanov and Reis (1995). Infarct volume, expressed in mm 3 was calculated by a linear integration of the corrected lesion areas, as previously described (Heurteaux et al, 2006a).…”

Section: Middle Cerebral Artery Occlusionmentioning

confidence: 99%

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Blondeau

Nguemeni

Debruyne

et al. 2009

Neuropsychopharmacol

122

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Omega-3 polyunsaturated fatty acids are known to have therapeutic potential in several neurological and psychiatric disorders. However, the molecular mechanisms of action underlying these effects are not well elucidated. We previously showed that alpha-linolenic acid (ALA) reduced ischemic brain damage after a single treatment. To follow-up this finding, we investigated whether subchronic ALA treatment promoted neuronal plasticity. Three sequential injections with a neuroprotective dose of ALA increased neurogenesis and expression of key proteins involved in synaptic functions, namely, synaptophysin-1, VAMP-2, and SNAP-25, as well as proteins supporting glutamatergic neurotransmission, namely, V-GLUT1 and V-GLUT2. These effects were correlated with an increase in brain-derived neurotrophic factor (BDNF) protein levels, both in vitro using neural stem cells and hippocampal cultures and in vivo, after subchronic ALA treatment. Given that BDNF has antidepressant activity, this led us to test whether subchronic ALA treatment could produce antidepressant-like behavior. ALA-treated mice had significantly reduced measures of depressive-like behavior compared with vehicletreated animals, suggesting another aspect of ALA treatment that could stimulate functional stroke recovery by potentially combining acute neuroprotection with long-term repair/compensatory plasticity. Indeed, three sequential injections of ALA enhanced protection, either as a pretreatment, wherein it reduced post-ischemic infarct volume 24 h after a 1-hour occlusion of the middle cerebral artery or as post-treatment therapy, wherein it augmented animal survival rates by threefold 10 days after ischemia.

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“…The lesion areas (in mm 2 ) were measured with an image analyzer (IMSTAR, Paris, France), and the distances between respective coronal sections were used to calculate the lesion volume. The brain lesion volume (in mm 3 ) was calculated by integrating the necrotic areas, corrected for edema, by the method of Golanov and Reis (1995).…”

Section: Brain Lesionmentioning

confidence: 99%

Combination Therapy with Fenofibrate, a Peroxisome Proliferator-Activated Receptor α Agonist, and Simvastatin, a 3-Hydroxy-3-methylglutaryl-Coenzyme A Reductase Inhibitor, on Experimental Traumatic Brain Injury

Chen

Besson²,

Béziaud³

et al. 2008

J Pharmacol Exp Ther

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We and others have demonstrated that fibrates [peroxisome proliferator-activated receptor (PPAR)␣ agonists] and statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) exerted neuroprotective and pleiotropic effects in experimental models of traumatic brain injury (TBI). Because the combination of statins and fibrates synergistically enhanced PPAR␣ activation, we hypothesized that the combination of both drugs may exert more important and/or prolonged beneficial effects in TBI than each alone. In this study, we examined the combination of fenofibrate with simvastatin, administered 1 and 6 h after injury, on the consequences of TBI. First, our dose-effect study demonstrated that the most efficient dose of simvastatin (37.5 mg/kg) reduced post-traumatic neurological deficits and brain edema. Then, the effects of the combination of fenofibrate (50 mg/kg) and simvastatin (37.5 mg/kg), given p.o. at 1 and 6 h after TBI, were evaluated on the TBI consequences in the early and late phase after injury. The combination exerted more sustained neurological recovery-promoting and antiedematous effects than monotherapies, and it synergistically decreased the post-traumatic brain lesion. Furthermore, a delayed treatment given p.o. at 3 and 8 h after TBI with the combination was still efficient on neurological deficits induced by TBI, but it failed to reduce the brain edema at 48 h. The present data represent the first demonstration that the combination of fenofibrate and simvastatin exerts prolonged and synergistic neuroprotective effects than each drug alone. Thus, these results may have important therapeutic significance for the treatment of TBI. Traumatic brain injury (TBI) remains one of the leading causes of death and disability in industrialized countries. Despite numerous studies on animal models of TBI that investigated therapeutic strategies, no neuroprotective therapy is currently available (Bramlett and Dietrich, 2004). TBI leads to important and deleterious neuroinflammation, as evidenced by edema, free radicals, cytokine production, induction of nitric-oxide synthase and cyclooxygenase type 2, and leukocyte infiltration. Strategies blocking each inflammatory and oxidative mediator have been shown to induce neuroprotective, anti-inflammatory and antioxidative effects after brain injury (Ray et al., 2002). Drugs that were able to modulate only one molecular pathway implicated in inflammation or oxidative stress induced beneficial effects in experimental studies, but they failed in clinical trials. Thus, one key to success in neuroprotection would be to simultaneously modulate many pathophysiological pathways with pharmacological agent inducing pleiotropic effects.One pleiotropic strategy is to activate peroxisome proliferator-activated receptor (PPAR) ␣. PPAR␣ is one of the three subtypes of the nuclear receptor PPAR family, which can be activated by natural ligands, such as polyunsaturated fatty acids, and synthetic ligands (drugs belonging to fibrate's family). PPARs are implicated in several...

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Contribution of Cerebral Edema to the Neuronal Salvage Elicited by Stimulation of Cerebellar Fastigial Nucleus after Occlusion of the Middle Cerebral Artery in Rat

Abstract: REFERENCES

Cited by 67 publications

References 22 publications

MLC901 Favors Angiogenesis and Associated Recovery after Ischemic Stroke in Mice

MLC901 Favors Angiogenesis and Associated Recovery after Ischemic Stroke in Mice

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Combination Therapy with Fenofibrate, a Peroxisome Proliferator-Activated Receptor α Agonist, and Simvastatin, a 3-Hydroxy-3-methylglutaryl-Coenzyme A Reductase Inhibitor, on Experimental Traumatic Brain Injury

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