Treadmill exercise improves memory function by inhibiting hippocampal apoptosis in pilocarpine-induced epileptic rats

Lee, Jae-Min; Ji, Eun‐Sang; Kim, Tae-Woon; Kim, Chang‐Ju; Shin, Mal‐Soon; Lim, Baek-Vin; Chung, Yong-Rak; Cho, Young‐Sam

doi:10.12965/jer.36394.197

Cited by 21 publications

(28 citation statements)

References 42 publications

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“…It is already well known that the number of live neurons decreases after a seizure (Kim et al, 2012;Jeong et al, 2017;Lee S. H. et al, 2018). Also, it is already well established that the number of apoptotic cells increases after a seizure (Lee J. M. et al, 2018;Li et al, 2019). To confirm the effects of cerebrolysin on neuronal death in a damaged hippocampus following a seizure, the density of live neurons was recorded to determine whether cerebrolysin treatment could rescue neuronal damage after a seizure.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

et al. 2020

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Epilepsy is one of the most common and severe brain diseases. The exact cause of epilepsy is unclear. Epilepsy often occurs following brain damage, such as traumatic brain injury (TBI) and ischemia. Cerebrolysin is a porcine brain peptide that is a unique neurotropic and neuroprotective agent. Cerebrolysin has been reported to increase neuroprotective effects after TBI, ischemia, and other CNS diseases. However, the effects of cerebrolysin on seizures are not known. Therefore, this study aimed to investigate the effects of neuropeptide cerebrolysin on neuronal death in the hippocampus after a seizure. To confirm the effects of cerebrolysin, we used a pilocarpine-induced seizure animal model. Cerebrolysin (2.5 ml/kg, i.p., once per day for 7 days) was immediately injected after a seizure induction. After 1 week, we obtained brain tissues and performed staining to histologically evaluate the potentially protective effects of cerebrolysin on seizure-induced neuronal death in the hippocampus. We found that cerebrolysin decreased hippocampal neuronal death after a seizure. In addition, an increase in brain-derived neurotrophic factor (BDNF) was confirmed through Western blot analysis to further support our hypothesis. Therefore, the present study suggests that the administration of cerebrolysin can be a useful therapeutic tool for preventing neuronal death after a seizure.

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Section: Discussionmentioning

confidence: 99%

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

et al. 2020

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“…The hippocampus is an important area of the brain that is involved in the process of learning and memory formation, and hippocampal nerve production continues to occur after the development of the nervous system ( López-Toledano and Shelanski, 2004 ). Doublecortin (DCX) is a marker of neuronal progenitor cells, and DCX is involved in neuronal migration and development ( Lee et al, 2018 ; Park et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of swimming exercise on social isolation-induced memory impairment and apoptosis in old rats

Park

Kim

et al. 2020

J Exerc Rehabil

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Effect of swimming exercise on serotonin (5-hydroxytryptamine, 5-HT) expression and apoptosis in social isolation rats during old age was investigated. Rats in the old social isolation groups were housed alone per cage for 4 weeks. Rats in the swimming exercise groups were allowed to swim for 30 min once daily for 4 weeks. Morris water maze task determined spatial working memory and elevated plus maze test determined anxiety. Immunohistochemistry for tryptophan hydroxylase (TPH) and 5-HT in the dorsal raphe and for doublecortin (DCX) in the hippocampal dentate gyrus was conducted. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining in the hippocampal dentate gyrus was performed. Western blot analysis for Bax, Bcl-2, and cytochrome c in the hippocampus was conducted. Social isolation in rats of old age reduced spatial working memory and increased anxiety level. Swimming exercise enhanced spatial working memory and suppressed anxiety level. Social isolation in rats of old age inhibited TPH and 5-HT expression in dorsal rape. Swimming exercise increased TPH and 5-HT expression. Social isolation in rats of old age inhibited DCX-positive cells in the hippocampal dente gyrus. Swimming exercise increased DCX-positive cells. Social isolation in rats of old age increased TUNEL-positive cells, Bax and cytochrome c expression, and decreased Bcl-2 expression, which promoted apoptosis. Swimming exercise suppressed TUNEL-positive cells, Bax and cytochrome c expression, and increased Bcl-2 expression, which inhibited apoptosis. Swimming exercise improved 5-HT expression and suppressed apoptosis to alleviate anxiety and memory impairment during old age.

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“…Several AChE inhibitors, such as tacrine, donepezil, rivastigmine, and carbamates in hospital are used to treat AD. Moreover, there are many studies investigating the hippocampal region of the brain in an attempt to find candidate drugs to improve memory or treat AD [26][27][28][29]. We observed that pretreatment with glycyrrhizic acid (10 mg/kg or 20 mg/ kg) could decrease the AChE activity in the hippocampal region of the brain in scopolamine-induced cognitive impairment mice models.…”

Section: Discussionmentioning

confidence: 81%

Effect of Glycyrrhizic Acid on Scopolamine-Induced Cognitive Impairment in Mice

2020

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Purpose: Cognitive impairment is one of the main symptoms of Alzheimer disease and other dementias. Glycyrrhiza uralensis is a natural product that has a protective effect against cognitive impairment. In this study, we investigated whether glycyrrhizic acid, among the main bioactive components of <i>Glycyrrhiza uralensis</i>, has a neuroprotective effect on scopolamine-induced cognitive impairment.Methods: Twenty-week-old male Institute of Cancer Research mice were used in this study. The scopolamine-induced cognitive impairment mice model was used. Glycyrrhizic acid was orally administered to mice once daily for 21 days, while scopolamine (1 mg/kg) treatment was delivered 30 minutes before behavioral tests. Donepezil (2 mg/kg) was used as a positive drug control. To evaluate the effect of glycyrrhizic acid, the following assessments were performed on hippocampal tissue: Y-maze test, acetylcholinesterase activity, antioxidant enzymes’ activity (superoxide dismutase, catalase). Western blotting for phosphor-extracellular signal-regulated kinase, P38, and c-Jun NH2-terminal kinase was conducted.Results: We found that glycyrrhizic acid administration significantly improved scopolamine-induced cognitive impairment in the Y-maze test. The acetylcholinesterase activity, superoxide dismutase, and catalase activity in the glycyrrhizic acid-treated group showed a significant reversal of cognitive impairment compared with the scopolamine-treated group.Conclusions: Our results suggest that glycyrrhizic acid has a neuroprotective effect on cognitive function in scopolamine-induced cognitive impairment.

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Treadmill exercise improves memory function by inhibiting hippocampal apoptosis in pilocarpine-induced epileptic rats

Cited by 21 publications

References 42 publications

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

Effects of swimming exercise on social isolation-induced memory impairment and apoptosis in old rats

Effect of Glycyrrhizic Acid on Scopolamine-Induced Cognitive Impairment in Mice

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