Effect of nicotinamide on epileptic activity in the cerebral cortex

Крыжановский, Г. Н.; Шандра, А. А.; Makul'kin, R. F.; Lobasyuk, B. A.; Godlevskii, L. S.

doi:10.1007/bf00833254

Cited by 4 publications

(4 citation statements)

References 8 publications

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“…NAm is also reported to be an anticonvulsant, 32,33 anticoagulant, 34 and angiogenic 35 agent and an inhibitor of lipid peroxidation. 33 Thus, there are numerous ways in which NAm could potentially act to protect against injury due to focal cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Mokudai

Ayoub

Sakakibara

et al. 2000

Stroke

130

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Background and Purpose-We have previously shown that nicotinamide (NAm) acutely reduces brain infarction induced by permanent middle cerebral artery occlusion (MCAo) in rats. In this study, we investigate whether NAm may protect against ischemia/reperfusion injury by improving sensory and motor behavior as well as brain infarction volumes in a model of transient focal cerebral ischemia. Methods-Forty-eight male Wistar rats were used, and transient focal cerebral ischemia was induced by MCAo for 2 hours, followed by reperfusion for either 3 or 7 days. Animals were treated with either intraperitoneal saline or NAm (500 mg/kg) 2 hours after the onset of MCAo (ie, on reperfusion). Sensory and motor behavior scores and body weight were obtained daily, and brain infarction volumes were measured on euthanasia. Results-Relative to treatment with saline, treatment with NAm (500 mg/kg IP) 2 hours after the onset of transient focal cerebral ischemia in Wistar rats significantly improved sensory (38%, PϽ0.005) and motor (42%, PϽ0.05) neurological behavior and weight gain (7%, PϽ0.05) up to 7 days after MCAo. The cerebral infarct volumes were also reduced 46% (PϽ0.05) at 3 days and 35% (Pϭ0.09) at 7 days after MCAo. Conclusions-NAm is a robust neuroprotective agent against ischemia/reperfusion-induced brain injury in rats, even when administered up to 2 hours after the onset of stroke. Delayed NAm treatment improved both anatomic and functional indices of brain damage. Further studies are needed to clarify whether multiple doses of NAm will improve the extent and duration of this neuroprotective effect and to determine the mechanism(s) of action underlying the neuroprotection observed. Because NAm is already used clinically in large doses and has few side effects, these results are encouraging for the further examination of the possible use of NAm as a therapeutic neuroprotective agent in the clinical treatment of acute ischemic stroke. (Stroke. 2000;31:1679-1685.)

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Section: Discussionmentioning

confidence: 99%

Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Mokudai

Ayoub

Sakakibara

et al. 2000

Stroke

130

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“…NAm is also a poly(ADP-ribose) polymerase (PARP) inhibitor, similar to other well-known agents, such as 3-aminobenzamide, 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl-1(2H)isoquinolinone, and GP-6150, all of which also reduce cerebral infarct volume in models of stroke. [15][16][17][18] Furthermore, NAm is a reported anticonvulsant, 19 anticoagulant, 20 and angiogenic agent. 21 It has been shown to attenuate lipid peroxidation, 22 stroke-induced increase in lactate in humans, 23 and inhibit inducible nitric oxide synthase mRNA.…”

Section: Discussionmentioning

confidence: 99%

Delayed Multidose Treatment with Nicotinamide Extends the Degree and Duration of Neuroprotection by Reducing Infarction and Improving Behavioral Scores up to Two Weeks Following Transient Focal Cerebral Ischemia in Wistar Rats

Maynard

Ayoub

Shen

2001

Annals of the New York Academy of Sciences

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A single, delayed dose of nicotinamide (NAm) was shown to be protective against focal cerebral ischemia in rats, but the protection was limited to three to seven days following stroke. The investigation reported here was conducted to examine if the use of multiple doses of NAm, administered after the onset of focal cerebral ischemia, would extend the duration of neuroprotection compared with a single dose treatment regimen. Male Wistar rats were subjected to transient focal cerebral ischemia by occluding the right middle cerebral artery (MCAo) for two hours. Following MCAo, motor and sensory behavioral tests were performed daily and the cerebral infarct volumes were measured at two weeks after sacrifice. Each animal was placed into one of four groups that received either normal saline alone (Group S), one (Group A), two (Group B), or three (Group C) doses of NAm (500 mg/kg). Each animal, therefore, received three treatments over two weeks, with the first dose administered intravenously two hours after the onset of MCAo. Single and multiple doses of NAm reduced the infarction (p < 0.01) and improved (p < 0.05) the neurologic sensory and motor behavior when compared with the saline‐treated animals up to two weeks after stroke. Moreover, animals that received multiple doses of NAm recuperated full motor function not different from normal, preoperative motor behavior. Delayed treatment with NAm given as multiple doses, therefore, further enhances the extent and duration of neuroprotection by significantly reducing cerebral infarct volumes, improving neurologic behavioral scores, and confers a complete motor recovery up to two weeks from the onset of focal cerebral ischemia in Wistar rats.

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“…Nicotinamide is a water soluble vitamin of the B-complex; which together with nicotinic acid belongs to vit.-B3 or vita;-PP. It has been reported to be an anticonvulsant, anticoagulant, angiogenic agent and an inhibitor of lipid peroxidation (Kryzhanovskii et al 1980). It is naturally present in animal products, whole cereals, nuts and legumes (Basu and Dickerson 1996).…”

mentioning

confidence: 99%

Mitodepressive and chromotoxic impact of nicotinamide on root meristems of Cyamopsis tetragonoloba L.

Kumar

Shikha

2012

Chromosome Botany

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The present study was undertaken to study the effect of nicotinamide at different concentrations viz.0.5%, 1.0%, 1.5%, 2.0% on root meristems of Cyamopsis tetragonoloba L. Mitotic study reveals various types of chromosomal aberrations like scattering(C-metaphase), precocious, unorientations, laggard, stickiness, bridges etc. Among these scattering was most prominent followed by precocious movement at metaphase and stickiness at anaphase. The AMI is expressed in terms of RDR while the chromosomal abnormalities in terms of RAR. The RDR considerably became more negative and RAR was increased along with increasing doses of nicotinamide. Increase in the negative value of RDR was directly proportional to the severity of the mitotic inhibition. Thus it was found that along with increasing treatment doses of nicotinamide the total abnormality percent increased and the active mitotic index decreased which shows potential toxicity of nicotinamide at their higher doses in this plant.

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Effect of nicotinamide on epileptic activity in the cerebral cortex

Cited by 4 publications

References 8 publications

Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Delayed Multidose Treatment with Nicotinamide Extends the Degree and Duration of Neuroprotection by Reducing Infarction and Improving Behavioral Scores up to Two Weeks Following Transient Focal Cerebral Ischemia in Wistar Rats

Mitodepressive and chromotoxic impact of nicotinamide on root meristems of Cyamopsis tetragonoloba L.

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Effect of nicotinamide on epileptic activity in the cerebral cortex

Cited by 4 publications

References 8 publications

Delayed Treatment With Nicotinamide (Vitamin B 3 ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Delayed Treatment With Nicotinamide (Vitamin B 3 ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Delayed Multidose Treatment with Nicotinamide Extends the Degree and Duration of Neuroprotection by Reducing Infarction and Improving Behavioral Scores up to Two Weeks Following Transient Focal Cerebral Ischemia in Wistar Rats

Mitodepressive and chromotoxic impact of nicotinamide on root meristems of Cyamopsis tetragonoloba L.

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Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats

Delayed Treatment With Nicotinamide (Vitamin B ₃ ) Improves Neurological Outcome and Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Wistar Rats