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PubMed2005

Inhibition of brain damage by edaravone, a free radical scavenger, can be monitored by plasma biomarkers that detect oxidative and astrocyte damage in patients with acute cerebral infarction.

We assess the availability of plasma biomarkers to monitor the brain damage and the therapeutic efficacy of edaravone. The study consisted of 51 patients with ischemic cerebral infarcts. They were divided into 2 groups: GI (n = 24) had cortical lesions, and GII (n = 27) had lesions in the basal ganglia or brain stem. Edaravone was administered to 27 randomly selected patients (GIa, n = 13; GIIa, n = 14) and its efficacy was studied by comparing their plasma OxLDL, S-100B, and MnSOD levels to those in patients without edaravone (GIb, n = 11, GIIb, n = 13). Three days after the start of edaravone, plasma OxLDL was significantly lower in GIa than GIb patients (0.177 +/- 0.024 ng/microg apoB vs 0.219 +/- 0.026, P < 0.05). In GIIa patients, pre- and posttreatment plasma OxLDL was not significantly different (0.156 +/- 0.013 vs 0.152 +/- 0.020). In GIa patients, S-100B and MnSOD were significantly lower than in GIb patients (P < 0.05). The neurological condition at the time of discharge had recovered in GIa but not GIb patients. Ours is the first evidence to confirm the efficacy of edaravone by plasma biomarkers. In patients with cortical infarcts, edaravone reduced oxidative damage, thereby limiting the degree of brain damage.

Adult↗

PubMedDate not supplied

A new free radical scavenger, edaravone, ameliorates oxidative liver damage due to ischemia-reperfusion in vitro and in vivo.

Ischemia-reperfusion injury causes oxidative stress producing reactive oxygen species, which is a serious problem linked to morbidity and mortality in liver surgery. We investigated the effects of edaravone, a new free radical scavenger, on liver oxidative stress in vitro and in vivo. We employed a hypoxia-reoxygenation model of primary cultured hepatocytes using an AnaeroPack (Mitsubishi Gas Chemical Co., Tokyo, Japan). Hepatocytes were exposed to 3 or 4 hours of hypoxia and then returned to oxygenation. We analyzed the time course changes of aspartate aminotransferase (AST), phosphatidylcholine hydroperoxide (PCOOH), and adenosine triphosphate (ATP) content in hepatocytes of edaravone-treated groups or nontreated groups after reoxygenation. Edaravone significantly attenuated the elevation of the AST level of the medium and hepatocellular PCOOH and preserved the hepatocellular ATP level. In vivo, male Sprague-Dawley rats were subjected to 45 minutes of hepatic ischemia and 120 minutes of reperfusion. The rats were intravenously injected with vehicle or edaravone (3 mg/kg or 10 mg/kg) before reperfusion and 1 hour after reperfusion. Serum AST levels and hepatic PCOOH and energy charge were significantly improved in both edaravone groups compared with control. In conclusion, edaravone has the ability to eliminate intra-hepatocellular superoxide species and attenuate oxidative liver damage in liver surgery.

Animals↗

PubMed2006

Effects of edaravone on N-methyl-D-aspartate (NMDA)-mediated cytochrome c release and apoptosis in neonatal rat cerebrocortical slices.

N-Methyl-D-aspartate-mediated neurotoxicity is known to involve nitric oxide production and to be augmented in an environment of reactive oxygen species. We used TUNEL staining and homogenous cytosolic immunoreactivity of cytochrome c in an acute brain slice preparation to investigate the influence of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, on N-methyl-D-aspartate-induced apoptosis. Cerebrocortical slices were obtained from parietal lobes of 7-day-old Sprague-Dawley rats, superfused with well-oxygenated artificial cerebrospinal fluid, and metabolically recovered. Subsequent 30-min exposures to 10 microM N-methyl-D-aspartate in treated and untreated slices were followed by 4 h of recovery superfusion with oxygenated artificial cerebrospinal fluid. Outcomes were compared for three groups of slices: "the N-methyl-D-aspartate-only group"; "the edaravone treatment group", which had 20 microM edaravone present throughout and subsequent to N-methyl-D-aspartate exposure; the "control group", in which slices were superfused only with oxygenated artificial cerebrospinal fluid. At the conclusion of recovery (t = 4 h), the percentage of TUNEL-positive cells in the edaravone treatment group (7.0+/-3.3%) was significantly reduced from the percentage for the N-methyl-D-aspartate-only group (21.9+/-4.1%), and insignificantly greater than the percentage for the control group (3.4+/-2.1%). Percentages of cytochrome c positive cells at t = 1 h were significantly increased (p < 0.01) in the N-methyl-d-aspartate-only group (30.6+/-1.9%) compared to percentages for both the control group (11.4+/-2.6%) and the edaravone treatment group (15.2+/-2.1%). Edaravone's reduction in TUNEL staining and cytochrome c release provides evidence of reactive oxygen species mechanisms and antioxidant benefits in cytochrome c-mediated apoptosis during N-methyl-D-aspartate excitotoxicity.

Animals↗

PubMed2006

Edaravone reduces ischemia-reperfusion injury mediators in rat liver.

BACKGROUND: In hepatic ischemia-reperfusion (I/R) injury, oxidative stress both directly injures the liver and promotes an inflammatory reaction by up-regulating various inflammatory mediators. We investigated whether edaravone, a new hydroxy radical scavenger, could reduce hepatic I/R injury including expression of inflammatory mediators such as cytokines and adhesion molecules. MATERIALS AND METHODS: Male Sprague-Dawley rats were subjected to 30 min of partial hepatic pedicle clamping (70%) followed by reperfusion. Just after initiation of reperfusion and again 1 h later, edaravone was administered intraportally. After reperfusion hepatic lipid peroxidation was measured by thiobarbituric acid assay, and hepatic injury was quantified by measuring hepatic enzymes in plasma. We serially quantified hepatic expression of mRNAs for tumor necrosis factor (TNF)-alpha and E-selectin, and histologically examined E-selectin expression and neutrophil accumulation. RESULTS: In the edaravone group, hepatic lipid peroxidation and hepatic enzyme leakage were significantly less than in the saline group. Hepatic expression of TNF-alpha and E-selectin mRNAs was significantly lower in the edaravone than the saline group, at 2 h after initiation of reperfusion. Histologically, E-selectin immunoreactivity and neutrophil accumulation were less evident in hepatic sections from the edaravone group. CONCLUSIONS: Edaravone reduced hepatic I/R injury by minimizing oxidative stress, and inhibited subsequent injurious inflammation by reducing expression of inflammatory cytokines and adhesion molecules.

Animals↗

PubMed2005

Experimental study on the protective effects of edaravone against ischemic spinal cord injury.

OBJECTIVE: Reactive free radical species are thought to be involved in ischemic spinal cord injury. We investigated the effects of edaravone (Mitsubishi Pharma Co, Tokyo, Japan), a free radical scavenger, on spinal ischemia-reperfusion injury in a rabbit model. We also sought to estimate free radicals in the spinal cord using the microdialysis method. METHODS: Spinal cord ischemia was induced in New Zealand White rabbits. The animals were then divided into 4 groups. In the first experiment, which was carried out in group A (non-edaravone treated) and group B (edaravone treated), we assessed neurologic function and evaluated spinal cord histopathology. In the second experiment, which was performed in group C (non-edaravone treated) and group D (edaravone treated), we sequentially estimated the level of free radical species in the spinal cord with the microdialysis method. RESULTS: In the first experiment group B showed better neurologic function than group A. The number of viable neurons in the spinal cord gray matter was also higher in group B than in group A. The second experiment revealed that the level of free radical species was lower in group D at 75, 90, and 150 minutes after the beginning of reperfusion compared with levels seen in group C. The appearance of free radical species in the latter group was found to have a biphasic pattern, with peaks at 75 and 150 minutes after the beginning of reperfusion. CONCLUSION: Edaravone exerted a significant protective effect on the spinal cord against ischemia-reperfusion injury by suppressing the level of free radical species, which was demonstrated with the microdialysis method.

Animals↗

PubMed2006

Edaravone attenuates hydroxyl radical stress and augmented angiotensin II response in diabetic rats.

Reactive oxygen species (ROS) potentiate angiotensin II (Ang II) responses in diabetic vasculature. However, superoxide scavengers partially restore this effect, suggesting free radicals other than superoxide could be involved. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) is an antioxidant, which primarily scavenges hydroxyl radicals and is approved for use in stroke patients. Hence, to evaluate the role of hydroxyl radical stress in diabetic vascular complications, we studied the effect of edaravone (3 mgkg(-1), i.p., b.i.d.) treatment on Ang II responses in thoracic aorta isolated from streptozotocin (60 mgkg(-1) i.p.) induced 8 weeks diabetic male Sprague-Dawley rats. Ang II (10(-10) to 10(-6)M), tert-butyl hydro peroxide (tBHP; 10(-6) to 10(-2)M) or hydrogen peroxide (H2O2; 10(-6) to 10(-3)M) induced contractile response was significantly enhanced in aortic strips from diabetic as compared to control rats. Lipid peroxidation was significantly enhanced while the superoxide dismutase (SOD) and catalase activity was significantly lower in aorta of diabetic rats as compared to control rats. Acute (in vitro) exposure of edaravone (10(-5)M) to aortic strips from diabetic rats in the organ bath restored the augmented Ang II but not tBHP or H2O2-induced contractile response. In vivo edaravone (3mgkg(-1), i.p., b.i.d.) treatment for 2 weeks selectively attenuated the augmented Ang II- but not tBHP- or H2O2-induced contractile response. The enhanced systolic pressure, lipid peroxidation and the reduced SOD and catalase activity were restored to control values following 2 weeks edaravone treatment. From our results we infer that hydroxyl radical stress augments Ang II response in diabetic rat thoracic aorta and edaravone could be an ideal antioxidant adjuvant in the therapy of diabetic vascular complications.

Angiotensin II↗

PubMed2004

Edaravone inhibits acute renal injury and cyst formation in cisplatin-treated rat kidney.

BACKGROUND: Although cis-diamminedichloroplatinum (II) (cisplatin) is an effective anticancer agent, its clinical use is highly limited predominantly due to its adverse effects on renal functions. The present work examined the therapeutic potential of edaravone, a free radical scavenger, for inhibiting cisplatin-induced renal injury. METHODS: Edaravone, 3-methyl-1-phenyl-pyrazolin-5-one, was administrated intravenously at a dose of 30 mg/kg of body weight to male Wistar rats (200-220 g). After 30 min, cisplatin was injected intraperitoneally at a dose of 5 mg/kg of body weight. At the indicated times after the treatment, functions and histological changes of the kidney were analyzed. To test the therapeutic potential of edaravone in chemotherapy, its effect on the anticancer action of cisplatin was examined in ascites cancer-bearing rats. RESULTS: We found that cisplatin rapidly impaired the respiratory function and DNA of mitochondria in renal proximal tubules, thereby inducing apoptosis of tubular epithelial cells within a few days and chronic renal dysfunction associated with multiple cysts one-year after the administration. Administration of edaravone inhibited the cisplatin-induced acute injury of mitochondria and their DNA and renal epithelial cell apoptosis as well as the occurrence of chronic renal dysfunction and multiple cyst formation. The anticancer effect of cisplatin remained unaffected by intravenous administrating of edaravone. CONCLUSIONS: These results indicate that edaravone may have therapeutic potential for inhibiting the acute and chronic injury of the kidney induced by cisplatin.

Animals↗

PubMed2006

Edaravone inhibits rheumatoid synovial cell proliferation and migration.

Rheumatoid arthritis (RA) is characterized by synovial proliferation and migration which is induced by proinflammatory cytokines or oxidative stress, followed by joint destruction. Edaravone, clinically available free radical scavenger in Japan, is confirmed to be beneficial in the acute stage of cerebral infarction. We aimed to investigate whether edaravone suppressed in vitro proliferation and migration of synovial cells (SC) induced by IL-1beta. SC proliferation and migration induced by IL-1beta were dose-dependently suppressed by edaravone at the clinically available concentration. These data suggest that edaravone has potential effects to suppress SC proliferation and migration, followed by suppression of synovial proliferation in RA. Therefore, edaravone, an antioxidant agent, might be a novel therapeutic agent which develops the new strategy for treatment of RA, and more detailed studies are required to establish the therapeutic effect of edaravone on RA in vivo.

Aged↗

PubMed2006

Electron spin resonance and spin trapping technique provide direct evidence that edaravone prevents acute ischemia-reperfusion injury of the liver by limiting free radical-mediated tissue damage.

A novel free radical scavenger, 3-methyl-1-phenyl-2-pyrazolin-5-one (edaravone), is used for the treatment of acute ischemic stroke and is protective in several animal models of organ injury. We tested whether edaravone is protective against acute liver warm ischemia/reperfusion injury in the rat by acting as a radical scavenger. When edaravone was administered prior to ischemia and at the time of initiation of the reperfusion, liver injury was markedly reduced. Production of oxidants in the liver in this model was assessed in vivo by spin-trapping/electron spin resonance (ESR) spectroscopy. Ischemia/reperfusion caused an increase in free radical adducts rapidly, an effect markedly blocked by edaravone. Furthermore, edaravone treatment blunted ischemia/reperfusion-induced elevation in pro-inflammatory cytokines, infiltration of leukocytes and lipid peroxidation in the liver. These results demonstrate that edaravone is an effective blocker of free radicals in vivo in the liver after ischemia/reperfusion, leading to prevention of organ injury by limiting the deleterious effects of free radicals.

Acute Disease↗

PubMed2005

Edaravone reduces early accumulation of oxidative products and sequential inflammatory responses after transient focal ischemia in mice brain.

BACKGROUND AND PURPOSE: Oxidative stress contributes to ischemia/reperfusion neuronal damage in a consecutive 2-phase pattern: an immediate direct cytotoxic effect and subsequent redox-mediated inflammatory insult. The present study was designed to assess the neuroprotective mechanisms of edaravone, a novel free radical scavenger, through antioxidative and anti-inflammatory pathways, from the early period to up to 7 days after ischemia/reperfusion in mice. METHODS: Mice were subjected to 60-minute ischemia followed by reperfusion. They were divided into the edaravone group (n=72; with different schedules for first administration) and the vehicle (control) group (n=36). Infarct volume and neurological deficit scores were evaluated at several time points after ischemia. Immunohistochemical analysis for 4-hydroxy-2-nonenal (HNE), 8-hydroxy-deoxyguanosine (8-OHdG), ionized calcium-binding adapter molecule 1 (Iba-1), inducible NO synthase (iNOS), and nitrotyrosine were performed at 24 hours, 72 hours, or 7 days after reperfusion. RESULT: Edaravone, even when administrated 6 hours after onset of ischemia/reperfusion, significantly reduced the infarct volume (68.10+/-6.24%; P<0.05) and improved the neurological deficit scores (P<0.05) at 24 hours after reperfusion. Edaravone markedly suppressed the accumulation of HNE-modified protein and 8-OHdG at the penumbra area during the early period after reperfusion (P<0.05) and reduced microglial activation, iNOS expression, and nitrotyrosine formation at the late period. CONCLUSIONS: Our results indicated that edaravone exerts an early neuroprotective effect through the early free radicals scavenging pathway and a late anti-inflammatory effect and suggested that edaravone is important for expansion of the therapeutic time window in stroke patients.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2005

Short-term administration of a new free radical scavenger, edaravone, is more effective than its long-term administration for the treatment of neonatal hypoxic-ischemic encephalopathy.

BACKGROUND AND PURPOSE: Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) is a new free radical scavenger that is used for the treatment of adult acute cerebral infarction in Japan. We examined the effect of edaravone on the optimal duration of treatment, the long-term effect on the brain, and the effect on learning and memory disability in a rat model of neonatal hypoxic-ischemic encephalopathy. METHODS: Seven-day-old Wistar rats were subjected to left common carotid artery ligation then 2 hours of hypoxic-ischemic insult or sham operation. Edaravone was administered intraperitoneally (9 mg/kg) after hypoxic-ischemic insult every 24 hours for 2, 5, or 10 consecutive days. The neuroprotective effect of edaravone was evaluated by behavioral test and histological analysis. RESULTS: Two-day treatment with edaravone significantly gave protection to the learning and memory capability, as well as morphological recovery compared with control rats. Five-day treatment showed morphological improvement but no behavioral improvement. In contrast, 10-day treatment did not show either morphological or behavior improvement. CONCLUSIONS: These findings indicate that edaravone is a promising candidate as a treatment of choice for neonatal hypoxic-ischemic encephalopathy, when its use is limited to the acute phase after hypoxia-ischemia.

Animals↗

PubMed2004

Pretreatment with the free radical scavenger edaravone prevents cerebral hyperperfusion after carotid endarterectomy.

OBJECTIVE: Cerebral hyperperfusion syndrome after carotid endarterectomy (CEA) is a rare but potentially devastating complication. The purpose of the present study, which was not a randomized controlled trial but a case cohort study with historical control, was to determine whether pretreatment with a novel free radical scavenger, edaravone, could prevent occurrence of cerebral hyperperfusion after CEA. METHODS: Fifty patients with ipsilateral internal carotid artery stenosis (>/=70%) underwent CEA with administration of edaravone before internal carotid artery clamping. Preoperative cerebral blood flow and cerebrovascular reactivity (CVR) to acetazolamide were assessed with single-photon emission computed tomography (SPECT). Cerebral blood flow also was measured immediately after CEA and on the 3rd postoperative day. RESULTS: Cerebral hyperperfusion (cerebral blood flow increase >/=100% compared with preoperative values) was revealed by SPECT performed immediately after CEA in only one patient (2%), who also exhibited reduced preoperative CVR. The incidence of post-CEA hyperperfusion as revealed by SPECT in the control group (51 CEA patients without administration of edaravone) was significantly higher (16%) (P = 0.0310, control versus treatment group). In addition, in a subgroup of patients with reduced preoperative CVR, the incidence of post-CEA hyperperfusion as revealed by SPECT in the edaravone group (7%) was significantly lower than that in the control group (67%) (P = 0.0029). Logistic regression analysis demonstrated that reduced preoperative CVR and absence of pretreatment with edaravone were significant independent predictors of post-CEA hyperperfusion as revealed by SPECT. CONCLUSION: Pretreatment with edaravone can prevent occurrence of cerebral hyperperfusion after CEA.

Aged↗

PubMed2004

[Alterations of antiproliferative effects of serum obtained from patients with acute cerebral infarction treated with a radical scavenger, edaravone, with or without amlodipine using an in vitro cultured basilar artery smooth muscle cells].

The guinea-pig basilar artery smooth muscle cell (GBa-SM3) culture system in the Dulbecco's modified Eagle's medium for 3 days serves as a useful in vitro model for assessing antiproliferative effects of various therapeutic agents on vessels. With use of this system we studied whether human serum obtained from patients with acute cerebral infarction (n = 16) would have a proliferative effect on vessels and whether an administration of a free radical scavenger, edaravone, with or without amlodipine would elicit antiproliferative effects. The control serum was obtained from 3 healthy human subjects. Time courses of the cell growth and survival were measured colorimetrically by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrzolium bromide (MTT) test. The stimulatory effect on the proliferation of GBa-SM3 cells of patients' serum obtained immediately after infarction was significantly (p < 0.05) greater than those obtained from the same patients after the treatment of edaravone for 2 weeks. In addition, the serum obtained from the patients treated by edaravone and amlodipine (n = 7) showed a significantly (p < 0.05) greater antiproliferative effect than that obtained from those treated by edaravone (n = 9). In conclusion, edaravone may have a clinically beneficial antiproliferative effect on vascular smooth muscle cells. Co-administration of amlodipine, possessing an antioxidative calcium channel blocker, with edaravone may be a promising combination to patients with acute cerebral infarction. Further controlled clinical trials with a large number of patients should be warranted.

Acute Disease↗

PubMed2002

[Pharmacological and clinical profile of the free radical scavenger edaravone as a neuroprotective agent].

The involvement of oxygen radical species has been implicated in ischemic and post-ischemic brain cell damage. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one; M.W. 174.20, MCI-186, Radicut Injection) has an inhibitory effect on lipid peroxidation by scavenging free radicals and prevents vascular endothelial cell injury. In rat brain ischemic models, post-ischemic treatment with edaravone reduces .OH production and infarction of the ischemic penumbral area and suppresses delayed neuronal death. It also improves neurological deficits and diminishes deterioration of brain edema observed after ischemia. We investigated the efficacy and safety of edaravone in acute ischemic stroke patients. Edaravone improved the core neurological deficits, impaired activities of daily living, and disability, without serious safety problems. Edaravone was approved in Japan for the treatment of acute brain infarction within 24 h after onset in April, 2001. We hope that edaravone represents a promising neuroprotective agent that can contribute to the treatment of acute ischemic stroke.

Animals↗

PubMed2003

The free radical scavenger edaravone suppresses experimental closed duodenal loop-induced acute pancreatitis in rats.

Recent studies suggest that the enhanced release of reactive oxygen species (ROS) plays an important role in the pathogenesis of clinical acute pancreatitis. In the present study, we investigated the effects of the free radical scavenger edaravone, which is used clinically as an anti-stroke agent, in the development of experimental closed duodenal loop (CDL)-induced acute pancreatitis. In the CDL-pancreatitis model, after edaravone and vehicle saline were injected intravenously, pancreatitis was induced for 7 h by the CDL technique. The subsequent ascites volume, wet pancreatic weight, serum amylase levels, and pancreatic tissue lipid peroxide levels were evaluated. Pancreatic tissue damage was also evaluated histologically. In this CDL-induced pancreatitis model, edaravone treatment tended to reduce the ascites volume and inhibit the increases in the wet pancreatic weight. Edaravone also tended to reduced the microscopic mucosal damage scores and pancreatic tissue lipid peroxide levels. In particular, the serum amylase levels in the edaravone-treated rats (1-20 mg/kg i.v.) were significantly reduced as compared to the vehicle-treated rats. These results strongly support the involvement of ROS in the pathogenesis of CDL-induced acute pancreatitis and cytoprotective effects of free radical scavender against pancreatic acinar cells. A clinical effect for edaravone against acute pancreatitis is strongly expected.

Aldehydes↗

PubMed2003

The free radical scavenger edaravone suppresses experimental dextran sulfate sodium-induced colitis in rats.

Recent studies suggest that the enhanced release of reactive oxygen species (ROS) plays an important role in the pathogenesis of clinical inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease. In the present study, we investigated the effects of the free radical scavenger edaravone, which is used clinically as an anti-stroke agent, in the development of experimental dextran sulfate sodium (DSS)-induced colitis in rats. The rats were fed 4% (w/w of diet) DSS in standard powder chow for 8 days. The edaravone and vehicle saline were injected subcutaneously twice a day. After the experimental period, the wet colonic weight, macroscopic mucosal damaged area, histological damage score, mucosal myeloperoxidase (MPO) activity, mucosal tissue lipid peroxidate and serum interleukin-6 (IL-6) levels were measured. In the DSS-induced colitis model, edaravone treatment (1-20 mg/kg day) significantly reduced the wet colonic weight, macroscopic damaged area, and the histological damage score. Edaravone treatment also reduced mucosal MPO activity, mucosal tissue lipid peroxidate level and serum IL-6 level. In particular, edaravone at a dose of 20 mg/kg day significantly reduced mucosal MPO activity and serum IL-6 level. These results strongly support the involvement of ROS in the pathogenesis of DSS-induced colitis. A clinical effect for edaravone against IBD patients is strongly expected.

Aldehydes↗

PubMed2003

Effect of a novel free radical scavenger, edaravone (MCI-186), on acute brain infarction. Randomized, placebo-controlled, double-blind study at multicenters.

Edaravone, a novel free radical scavenger, demonstrates neuroprotective effects by inhibiting vascular endothelial cell injury and ameliorating neuronal damage in ischemic brain models. The present study was undertaken to verify its therapeutic efficacy following acute ischemic stroke. We performed a multicenter, randomized, placebo-controlled, double-blind study on acute ischemic stroke patients commencing within 72 h of onset. Edaravone was infused at a dose of 30 mg, twice a day, for 14 days. At discharge within 3 months or at 3 months after onset, the functional outcome was evaluated using the modified Rankin Scale. Two hundred and fifty-two patients were initially enrolled. Of these, 125 were allocated to the edaravone group and 125 to the placebo group for analysis. Two patients were excluded because of subarachnoid hemorrhage and disseminated intravascular coagulation. A significant improvement in functional outcome was observed in the edaravone group as evaluated by the modified Rankin Scale (p = 0.0382). Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.

Acute Disease↗

PubMed2006

Inhibitory effects of edaravone on the production of tumor necrosis factor-alpha in the isolated heart undergoing ischemia and reperfusion.

We evaluated the effects of edaravone, a hydroxyl radical scavenging agent, on the production of tumor necrosis factor-alpha (TNF-alpha) in myocardium, and the release of TNF-alpha and P-selectin from myocardium after ischemia-reperfusion injury in isolated Langendorff-perfused rat hearts. Cardiodynamic function at stable points during perfusion and 5, 15, 30, and 60 min after the initiation of reperfusion was evaluated by left ventricular developed pressure, rate of increase in left ventricular pressure and rate of decrease in ventricular pressure, coronary flow, and heart rate. At 60 min after the initiation of reperfusion, myocardial infarct size was estimated microscopically using triphenyltetrazolium chloride staining, and expression of TNF-alpha in myocardium was detected by Western blot and immunohistochemistry. At the same time points as the measurement of cardiodynamic function, TNF-alpha and the soluble form of P-selectin in coronary effluent were measured by enzyme immunoassay. At all time points during reperfusion, edaravone markedly improved cardiodynamic function and reduced myocardial infarct size in comparison to the control. In myocardium in the control, TNF-alpha was detected in the endothelial cells and other cells bearing some resemblance to interstitial cells and monocyte cells. Edaravone suppressed this cytokine expression in the corresponding sites. P-selectin as well as TNF-alpha was found in the coronary effluent of the control, and edaravone significantly decreased soluble P-selectin levels in comparison to the control (P < 0.01). Edaravone might have protective effects on cardiac function through reduction of infarct size via decrease of production of TNF-alpha in myocardium induced by ischemia-reperfusion injury and through reduction of the release of adhesion molecules such as P-selectin from vascular endothelial cells.

Analysis of Variance↗