The effect of crocin on memory, hippocampal acetylcholine level, and apoptosis in a rat model of cerebral ischemia

Yuan, Yu; Shan, Xiaosong; Men, Weidong; Zhai, Hexin; Qiao, Xiaoxia; Geng, Lianting; Li, Chunhui

doi:10.1016/j.biopha.2020.110543

Cited by 34 publications

(26 citation statements)

References 32 publications

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“…The mechanisms of post-ischemic brain neurodegeneration with the development of full-blown dementia are complex and unclear, influenced by multiple mediators. It has been suggested that changes in calcium levels, hyperactivity of the glutamate system, acetylcholine deficiency, and metal ion dyshomeostasis are closely related to post-ischemic neurodegenerative pathways [ 23 , 24 , 25 , 26 ]. In addition, processes such as oxidative stress, apoptosis, neuroinflammatory changes, and impaired autophagy have been shown to cause severe brain damage and contribute to chronic and irreversible changes following transient focal or global ischemia [ 16 , 17 , 27 , 28 , 29 , 30 , 31 , 32 ].…”

Section: Introductionmentioning

confidence: 99%

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Pluta

Czuczwar

Januszewski

et al. 2021

Cells

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Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified tau protein in a manner typical of Alzheimer’s disease neuropathology. Pathological changes in the tau protein, at the gene and protein level due to cerebral ischemia, can lead to the development of Alzheimer’s disease-type neuropathology and dementia. Some studies have shown increased tau protein staining and gene expression in neurons following ischemia-reperfusion brain injury. Recent studies have found the tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity, neuroinflammation, blood-brain barrier permeability, mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the tau protein in the brain. The tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following ischemia. The data indicate that an episode of cerebral ischemia activates the damage and death of neurons in the hippocampus in a tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following ischemia. In this review, we update our understanding of proteomic and genomic changes in the tau protein in post-ischemic brain injury and present the relationship between the modified tau protein and post-ischemic neuropathology and present a positive correlation between the modified tau protein and a post-ischemic neuropathology that has characteristics of Alzheimer’s disease-type neurodegeneration.

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Section: Introductionmentioning

confidence: 99%

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Pluta

Czuczwar

Januszewski

et al. 2021

Cells

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“…In particular, crocins (injected intraperitoneally) were found to exert an inhibitory action on acetylcholinesterase activity [39] and demonstrated efficacy in counteracting β-amyloid (Aβ)-induced cognitive deficits [40] and c-fos overexpression in rats [41]. In this context, it has been revealed that the oral administration of crocins conferred neuroprotection in a rat model of cerebral ischemia [42].…”

Section: Discussionmentioning

confidence: 99%

Crocins, the Bioactive Components of Crocus sativus L., Counteract the Disrupting Effects of Anesthetic Ketamine on Memory in Rats

Pitsikas

Tarantilis

2021

Molecules

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Consistent experimental evidence suggests that anesthetic doses of the non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist ketamine cause severe memory impairments in rodents. Crocins are among the various bioactive ingredients of the plant Crocus sativus L., and their implication in memory is well-documented. It has not yet been elucidated if crocins are able to attenuate the memory deficits produced by anesthetic ketamine. The present study was undertaken aiming to clarify this issue in the rat. For this aim, the object recognition, the object location and the habituation tests, reflecting non-spatial recognition memory, spatial recognition memory and associative memory, respectively, were utilized. A post-training challenge with crocins (15–30 mg/kg, intraperitoneally (i.p.), acutely) counteracted anesthetic ketamine (100 mg/kg, i.p.)-induced performance impairments in all the above-mentioned behavioral memory paradigms. The current findings suggest that crocins modulate anesthetic ketamine’s amnestic effects.

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“…The cleavage of calpain-related protein contributes to the loss of pyramidal neurons in the hippocampus following ischemia [ 43 ]. Following cerebral ischemia, loss of the pyramidal neurons in the CA1 region is apparent, along with a decline in acetylcholine levels in the hippocampus [ 44 ]. This suggests that the death of pyramidal neurons is also due to the inability of the hippocampus to transmit excitatory and cholinergic transmission to neurons [ 9 , 44 , 45 ].…”

Section: Neurodegenerative Changes In Post-ischemic Hippocampusmentioning

confidence: 99%

Post-Ischemic Neurodegeneration of the Hippocampus Resembling Alzheimer’s Disease Proteinopathy

Pluta

Januszewski

Czuczwar

2021

IJMS

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In this review, we summarize, inter alia, the protein and gene changes associated with Alzheimer’s disease and their role in post-ischemic hippocampal neurodegeneration. In the hippocampus, studies have revealed dysregulation of the genes for the amyloid protein precursor metabolism and tau protein that is identical in nature to Alzheimer’s disease. Data indicate that amyloid and tau protein, derived from brain tissue and blood due to increased permeability of the blood–brain barrier after ischemia, play a key role in post-ischemic neurodegeneration of the hippocampus, with concomitant development of full-blown dementia. Thus, the knowledge of new neurodegenerative mechanisms that cause neurodegeneration of the hippocampus after ischemia, resembling Alzheimer’s disease proteinopathy, will provide the most important therapeutic development goals to date.

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The effect of crocin on memory, hippocampal acetylcholine level, and apoptosis in a rat model of cerebral ischemia

Cited by 34 publications

References 32 publications

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Crocins, the Bioactive Components of Crocus sativus L., Counteract the Disrupting Effects of Anesthetic Ketamine on Memory in Rats

Post-Ischemic Neurodegeneration of the Hippocampus Resembling Alzheimer’s Disease Proteinopathy

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