Amelioration of cognitive deficits by Spirulina platensis in L-methionine-induced rat model of vascular dementia

Wang, Pian; Wang, Yan; Zhang, Qingbin; Li, Zheng; Li, Xiaoying; Kaur, Lavleen; Kumar, Manish

doi:10.4103/pm.pm_438_19

Cited by 9 publications

(4 citation statements)

References 61 publications

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“…Moreover, treatment with Sargassum extract both the dose (200mg/kg and 400mg/kg) significantly improved L-methionine induced endothelial dysfunction as measured in the terms of increased serum nitrite levels and decreased oxidative stress markers (decrease TBARS and increase, GSH). This experimental corroborated with Wang Pian et al finding amelioration of Spirulina platensis in L-methionine vascular dementia [34]. Meanwhile, the histological evidences showed pre-treatment with S. wightii 200mg/kg and 400mg/kg showed no sign neurodegeneration and neuron arrangement with normal structural integrity in the cortex hippocampus.…”

Section: Discussionsupporting

confidence: 82%

Effects of Sargassum wightii Methanolic Extract on L-Methionine Induced Experimental Vascular Dementia like Syndrome in Albino Wistar Rats

Rout

Rath

Bhattamisra

et al. 2021

JPRI

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Sargassum wightii is brown seaweeds with high nutritive value with natural bioactive compounds having diverse therapeutic activity. In recent years, research on Sargassum wightii has gain much interest in neuropharmacological field. Basing on neuroprotective effect of Sargassum wightii against Parkinson’s disease animal models, the possible protective effect on dementia is hypothesised. Addressing this question the present study was designed to investigate the effect of S. wightii on L-methionine induced vascular dementia like syndrome in male wistar albino rats. Vascular dementia was induced by oral administration of L-methionine (1.7 g/kg) per body weight for 4weeks S. wightii was given from day1 to day32. The neurobehavioral assessment was performed by Morris water maze test for learning and memory ability and blood sample was collected for serum nitrite and homocysteine analysis. The whole brain content was subjected to a series of biochemical analysis that included brain cholinesterase, malondialdehyde, reduced glutathione and histopathological examination. L-methionine impaired learning and memory, increased serum homocysteine and decreased serum nitrite level significantly (p<0.001). It also increased brain thiobarbituric acid reactive substances, reduced glutathione and increased acetylcholinesterase activity significantly (p<0.001). Sargassum wightii at 200mg/kg and 400mg/kg body weight reversed the L-methionine induced learning and memory deficits (p<0.01) and (p<0.001) respectively. The L-methionine induced biochemical alterations in serum and brain as well as histopathological aberration in cortex and hippocampus were restored by Sargassum wightii (p<0.01). This study concluded that Sargassum wightii ameliorated L-methionine induced vascular dementia like syndrome and provided a new concept in anti-dementia therapy as a neuroprotectants.

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Section: Discussionsupporting

confidence: 82%

Effects of Sargassum wightii Methanolic Extract on L-Methionine Induced Experimental Vascular Dementia like Syndrome in Albino Wistar Rats

Rout

Rath

Bhattamisra

et al. 2021

JPRI

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“…Vascular dementia (VaD) is caused by cumulative hippocampal neuronal damage caused by vascular factors [ 2 ]. Several risk factors are associated with VaD, including cardiovascular abnormalities, dyslipidaemia, obesity, smoking, diabetes, and increased homocysteine (Hcy) level [ 3 ]; targeting these risk factors will minimize the burden. One of the major risk factors for VaD is hyperhomocysteinemia (HHcy) [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Sitagliptin Attenuates the Cognitive Deficits in L‐Methionine‐Induced Vascular Dementia in Rats

Khodir

Faried

Abd-Elhafiz

et al. 2022

BioMed Research International

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Vascular dementia (VaD) is the second most prevalent type of dementia characterized by progressive cognitive deficits and is a major risk factor for the development of Alzheimer’s disease and other neurodegenerative disorders. This study is aimed at determining the potential neuroprotective effect of sitagliptin (STG) on cognitive deficits in L-methionine-induced VaD in rats and the possible underlying mechanisms. 30 adult male Wistar albino rats were divided equally ( n = 10 ) into three groups: control, VaD, and VaD + STG groups. The cognitive performance of the animals was conducted by open field, elevated plus maze, Y-maze, novel object recognition, and Morris water maze tests. Serum homocysteine, TNF-α, IL-6, IL-10, total cholesterol, and triglycerides levels were assessed together with hippocampal MDA, SOD, and BDNF. Histopathological and immunohistochemical assessments of the thoracic aorta and hippocampus (CA1 region) were also performed. Chronic L-methionine administration impaired memory and learning and induced anxiety. On the other hand, STG protected against cognitive deficits through improving oxidative stress biomarkers, inflammatory mediators, lipid profiles, and hippocampus level of BDNF as well as decreasing caspase-3 and GFAP and increasing Ki-67 immunoreactions in the hippocampus. Also, STG improved the endothelial dysfunction via upregulation of aortic eNOS immunoreaction. STG improved the cognitive deficits of L-methionine-induced VaD by its antioxidant, anti-inflammatory, antiapoptotic, and neurotrophic effects. These findings suggest that STG may be a promising future agent for protection against VaD.

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“…The increase in COX-2 appeared 21 days after the rats were given colchicine. L-methionine is also capable of causing neurodegeneration in CNS nerve cells after 12 weeks of treatment (Wang et al, 2020). This neurodegeneration is caused by neuroinflammation due to increased astrogliosis and microgliosis activity.…”

Section: Figure 5: Mechanism Of Lysolecithin Induced Msmentioning

confidence: 99%

Neurotoxin-induced animal model of multiple sclerosis: Molecular mechanism focus

Permana,

Siswanto,

Aziz

et al. 2024

Pharm Educ

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Background: Neurotoxins can alter the central nervous system. They induce severe clinical symptoms such as encephalopathy, convulsions, muscle paralysis, and respiratory failure. Hence, the neurotoxin can mimic human central nervous system disorders such as Multiple Sclerosis (MS) to study pathophysiology and drugs of development. Objective: This mini-review compared the neurotoxins for mimicking MS in animal models. Method: This study was a narrative review using the scientific electronic databases Scopus, PubMed, and Google Scholar. All related articles by keywords animal models, multiple sclerosis, and neurotoxins were collected by YP and BW. All authors contributed to manuscript development. Result: Cuprizone, ethidium bromide, lysolecithin, Myelin Oligodendrocyte Glycoprotein (MOG), and Myelin Essential Protein (MBP) are neurotoxins for MS animal models. Cuprizone is particularly relevant for use in studies addressing toxic mechanisms of the demyelination process and studies of therapeutic interventions. Ethidium bromide causes spinal cord demyelination with distinctive features in the oligodendrocytes and astrocytes. However, it is a carcinogen agent. Lysolecithin is suitable for old animal models because the duration for remyelination is relatively longer than others. MOG and MBP are preferable to resemble MS pathophysiology in humans. Conclusion: MOG and MBP are appropriate for generating animal multiple sclerosis models for further in vivo experiments.

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Amelioration of cognitive deficits by Spirulina platensis in L-methionine-induced rat model of vascular dementia

Cited by 9 publications

References 61 publications

Effects of Sargassum wightii Methanolic Extract on L-Methionine Induced Experimental Vascular Dementia like Syndrome in Albino Wistar Rats

Effects of Sargassum wightii Methanolic Extract on L-Methionine Induced Experimental Vascular Dementia like Syndrome in Albino Wistar Rats

Sitagliptin Attenuates the Cognitive Deficits in L‐Methionine‐Induced Vascular Dementia in Rats

Neurotoxin-induced animal model of multiple sclerosis: Molecular mechanism focus

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