Inducible nitric oxide inhibitor aminoguanidine, ameliorates deleterious effects of lipopolysaccharide on memory and long term potentiation in rat

Anaeigoudari, Akbar; Soukhtanloo, Mohammad; Reisi, Parham; Beheshti, Farimah; Hosseini, Mahmoud

doi:10.1016/j.lfs.2016.06.019

Cited by 54 publications

(29 citation statements)

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“…Considering these facts, it seems that an excessive production of proinflammatory cytokines followed by injection of LPS plays an important role in spatial memory and synaptic plasticity deficits caused by LPS in the present study. Supporting this idea, we have previously shown that administration of LPS (1 mg/kg) increases serum TNF α levels [10, 16, 31]. …”

Section: Discussionmentioning

confidence: 92%

Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Abareshi

Anaeigoudari

Norouzi

et al. 2016

Advances in Medicine

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Introduction. Renin-angiotensin system has a role in inflammation and also is involved in many brain functions such as learning, memory, and emotion. Neuroimmune factors have been proposed as the contributors to the pathogenesis of memory impairments. In the present study, the effect of captopril on spatial memory and synaptic plasticity impairments induced by lipopolysaccharide (LPS) was investigated. Methods. The rats were divided and treated into control (saline), LPS (1 mg/kg), LPS-captopril (LPS-Capto; 50 mg/kg captopril before LPS), and captopril groups (50 mg/kg) before saline. Morris water maze was done. Long-term potentiation (LTP) from CA1 area of hippocampus was assessed by 100 Hz stimulation in the ipsilateral Schaffer collateral pathway. Results. In the LPS group, the spent time and traveled path to reach the platform were longer than those in the control, while, in the LPS-Capto group, they were shorter than those in the LPS group. Moreover, the slope and amplitude of field excitatory postsynaptic potential (fEPSP) decreased in the LPS group, as compared to the control group, whereas, in the LPS-Capto group, they increased compared to the LPS group. Conclusion. The results of the present study showed that captopril improved the LPS-induced memory and LTP impairments induced by LPS in rats. Further investigations are required in order to better understand the exact responsible mechanism(s).

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Section: Discussionmentioning

confidence: 92%

Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Abareshi

Anaeigoudari

Norouzi

et al. 2016

Advances in Medicine

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“…It has been demonstrated that excessive production of free radicals and brain oxidative damage result in learning and memory deficits, and compounds with antioxidant properties can improve these processes 17 . Previously, we demonstrated the role of brain tissue oxidative damage in learning and memory deficits in rats 15 . Oxidative stress followed by PTU administration has also been suggested to have negative effects on learning and memory…”

Section: Discussionmentioning

confidence: 94%

“…On the probe day (sixth day), the platform was removed and the animals were allowed to swim for 60 seconds. The time spent and distance traveled in the target quadrant were recorded to compare between the groups 15 .…”

Section: Morris Water Maze Testmentioning

confidence: 99%

Thymoquinone reverses learning and memory impairments and brain tissue oxidative damage in hypothyroid juvenile rats

Baghcheghi

Hosseini

Beheshti

et al. 2018

Arq. Neuro-Psiquiatr.

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In this study, the effect of thymoquinone (TQ) on propylthiouracil (PTU)-induced memory impairment was investigated in juvenile rats. The rats were grouped into control, Hypo, Hypo-TQ5 and Hypo-TQ10. Propylthiouracil increased latency time in the Morris water maze test and decreased delay in entering the dark compartment in the passive avoidance test. Both 5 mg/kg and 10 mg/kg doses of TQ decreased latency time in the Morris water maze test and increased delay in entering the dark compartment in a passive avoidance test. The PTU also increased malondialdehyde and nitric oxide metabolites in the brain while reduced the thiol content and superoxide dismutase and catalase activities and serum T4 level. Both doses of TQ decreased malondialdehyde and nitric oxide metabolites in the brain while enhanced the thiol content and superoxide dismutase and catalase activities and serum T4 level. The results of the present study showed that TQ protected against PTU-induced memory impairments in rats.Keywords: hypothyroidism; propylthiouracil; memory RESUMO Neste estudo, foi investigado o efeito da timoquinona (TQ) contra deficiências de memória induzidas por propiltiouracilo (PTU) em ratos juvenis. Os ratos foram agrupados em grupos: controle, Hypo, Hypo-TQ5, e Hypo-TQ10. O PTU aumentou o tempo de latência no teste do labirinto aquático de Morris (MWM) e diminuiu o atraso para entrar no compartimento escuro no teste de evasão passiva (PA). Ambas as doses de TQ diminuíram o tempo de latência no teste de MWM e aumentaram o atraso para entrar no compartimento escuro no teste de PA. O PTU também aumentou os metabolitos de malondialdeído (MDA) e óxido nítrico (NO) no cérebro, enquanto reduziu o teor de tiol e as atividades de superóxido dismutasa (SOD) e catalasa (CAT) e o nível sérico de T4. Ambas as doses de TQ diminuíram os metabolitos de MDA e de NO no cérebro, aumentaram o conteúdo de tiol e as atividades de SOD e CAT e o nível de T4 no soro. Os resultados do presente estudo mostraram que a TQ protegeu contra deficiências de memória induzidas por PTU em ratos.

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“…These include lipopolysaccharide (LPS)-, polyI C-, streptozotocin-, okadaic acid-and colchicine-induced neuroinflammation. LPS-induced neuroinflammation represents the current standard paradigm to study neuroinflammation both in vivo (Hauss-Wegrzyniak et al 1998, Sheng et al 2003, Anaeigoudari et al 2016) and in vitro (Candiracci et al 2012. There are several other non-genetically manipulated rat models of AD which are not limited to induced neuroinflammation.…”

Section: Non-genetically Manipulated Neuro-inflammation Models For Admentioning

confidence: 99%

Lipopolysaccharide-Induced Memory Impairment in Rats: a Model of Alzheimer’s Disease

Yaacob²,

et al. 2017

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Alzheimer’s disease (AD) is a primary cause of dementia in the middle-aged and elderly worldwide. Animal models for AD are widely used to study the disease mechanisms as well as to test potential therapeutic agents for disease modification. Among the non-genetically manipulated neuroinflammation models for AD, lipopolysaccharide (LPS)-induced animal model is commonly used. This review paper aims to discuss the possible factors that influence rats’ response following LPS injection. Factors such as dose of LPS, route of administration, nature and duration of exposure as well as age and gender of animal used should be taken into account when designing a study using LPS-induced memory impairment as model for AD.

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Inducible nitric oxide inhibitor aminoguanidine, ameliorates deleterious effects of lipopolysaccharide on memory and long term potentiation in rat

Cited by 54 publications

References 54 publications

Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Thymoquinone reverses learning and memory impairments and brain tissue oxidative damage in hypothyroid juvenile rats

Lipopolysaccharide-Induced Memory Impairment in Rats: a Model of Alzheimer’s Disease

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