Docosahexaenoic acid and phosphatidylserine supplementations improve antioxidant activities and cognitive functions of the developing brain on pentylenetetrazol-induced seizure model

Liu, Shyh-Hwa; Chang, Ching Hsun; Chen, Pi-Hang; Su, Jheng-Ren; Chen, Chih‐Cheng; Chaung, Hso-Chi

doi:10.1016/j.brainres.2012.02.060

Cited by 42 publications

(42 citation statements)

References 34 publications

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“…It is clear that AD development is related to peroxidation of brain cells damaged by free radicals, obvious inflammatory reaction, and increased acetylcholine, which is consistent with the clinicopathological features of AD patients. AD rats given PS (15 or 30 mg/kg) showed significantly decreased escape latency in the Morris water maze and increased levels of SOD in the brain and improve hippocampal area pathology, which is consistent with results in the literature (Liu et al, 2012). Therefore, PS has an antioxidant function.…”

Section: Discussionsupporting

confidence: 91%

Effect of phosphatidylserine on memory in patients and rats with Alzheimer’s disease

Zhang¹,

Yang²,

Guo³

2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to investigate the effect of phosphatidylserine (PS) on memory of patients and rats with Alzheimer's disease (AD). In total, 57 AD patients were recruited from our hospital, and were divided into two groups: 25 in the control group and 32 in the observation group. Next, 300 mg/d of PS was given to the rats in the observation group for 12 continuous weeks based on the control group. AD rats were divided into three groups: control group, PS 30 mg/kg group, and PS 15 mg/kg group. Learning memory ability and free radical levels in the brain were detected after treatment. In AD patients, vocabulary and picture matching scores in the two treatment groups increased after treatment (P < 0.05). Moreover, the scores in the treated group were significantly greater than the control group (P < 0.05). In AD rats, PS treatment reduced the escape latent period of AD rats, increased SOD and OH -, and decreased acetylcholinesterase levels (P < 0.05). Compared with PS 15 mg/kg, PS 30 mg/kg group was significantly more efficacious (P < 0.05). Compared with the AD model group, hippocampal cells showed normal arrangement, karyopyknosis decreased, and the pathological changes in the two PS groups were considerable. In conclusion, PS decreased cholinesterase, improved memory, and improved hippocampal inflammation injury in AD brains by increasing SOD and OH -levels.

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Section: Discussionsupporting

confidence: 91%

Effect of phosphatidylserine on memory in patients and rats with Alzheimer’s disease

Zhang¹,

Yang²,

Guo³

2015

Genet. Mol. Res.

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“…The neuroprotective effect of OM3 and its constituents DHA and EPA in preventing seizures and cognitive impairments has been previously reported [4,6]. However, contradictory results have been published about the effective dose levels of OM3 or its constituents in this regard.…”

Section: Discussionmentioning

confidence: 99%

Omega-3 polyunsaturated fatty acids in large doses attenuate seizures, cognitive impairment, and hippocampal oxidative DNA damage in young kindled rats

Abdel-Wahab¹,

Alqahtani²,

El-Safty³

2015

Neuroscience Letters

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“…Following kainate injection, there is an increased oxidative stress, and development of seizures is also associated with such stressful condition (Liu et al, 2012). On the other hand, deficiency of antioxidant redox systems could exacerbate the etiology of epilepsy (Verrotti et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Kiasalari

Roghani

Khalili

et al. 2013

Pharmaceutical Biology

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Context: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Curcumin is the bioactive component of turmeric with anti-epileptic and neuroprotective potential. Objective: The beneficial effect of curcumin on the intrahippocampal kainate-induced model of TLE was investigated. Materials and methods: Rats were divided into sham, curcumin-pretreated sham, kainate and curcumin-pretreated kainate groups. The rat model of TLE was induced by unilateral intrahippocampal injection of 4 mg of kainate. Rats received curcumin p.o. at a dose of 100 mg/kg/d starting 1 week before the surgery. Seizure activity (SE) and oxidative stressrelated markers were measured. Furthermore, the Timm index for evaluation of mossy fiber sprouting (MFS) and number of Nissl-stained neurons were quantified. Results: All rats in the kainate group had SE, while 28.5% of rats showed seizures in the curcumin-pretreated kainate group. Malondialdehyde and nitrite and nitrate levels significantly increased in the kainate group (p50.01 and p50.05, respectively), and curcumin significantly lowered these parameters (p50.05). Superoxide dismutase activity significantly decreased in the kainate group (p50.05) and curcumin did not improve it. Rats in the kainate group showed a significant reduction of neurons in Cornu Ammonis 1 (CA1) (p50.05), CA3 (p50.005) and hilar (p50.01) regions, and curcumin significantly prevented these changes (p50.05-0.005). The Timm index significantly increased in the kainate group (p50.005), and curcumin significantly lowered this index (p50.01). Discussion and conclusion: Curcumin pretreatment can attenuate seizures, lower some oxidative stress markers, and prevent hippocampal neuronal loss and MFS in the kainate-induced model of TLE.

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Docosahexaenoic acid and phosphatidylserine supplementations improve antioxidant activities and cognitive functions of the developing brain on pentylenetetrazol-induced seizure model

Cited by 42 publications

References 34 publications

Effect of phosphatidylserine on memory in patients and rats with Alzheimer’s disease

Effect of phosphatidylserine on memory in patients and rats with Alzheimer’s disease

Omega-3 polyunsaturated fatty acids in large doses attenuate seizures, cognitive impairment, and hippocampal oxidative DNA damage in young kindled rats

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

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