Protective effects of melatonin against valproic acid-induced memory impairments and reductions in adult rat hippocampal neurogenesis

Neuroscience ◽  
2019 ◽  
Vol 406 ◽  
pp. 580-593 ◽  
Author(s):  
Anusara Aranarochana ◽  
Pornthip Chaisawang ◽  
Apiwat Sirichoat ◽  
Wanassanun Pannangrong ◽  
Peter Wigmore ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Hippocampal Neurogenesis ◽  
Protective Effects ◽  
Memory Impairments ◽  
Adult Rat

scholarly journals Hesperidin Reduces Memory Impairment Associated with Adult Rat Hippocampal Neurogenesis Triggered by Valproic Acid

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4364
Author(s):  
Anusara Aranarochana ◽  
Soraya Kaewngam ◽  
Tanaporn Anosri ◽  
Apiwat Sirichoat ◽  
Wanassanun Pannangrong ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Memory Impairment ◽  
Memory Loss ◽  
Hippocampal Neurogenesis ◽  
Immunofluorescent Staining ◽  
Ki 67 ◽  
Novel Object ◽  
Memory Impairments ◽  
Adult Rat ◽  
Behavioral Expression

Treatment with valproic acid (VPA) deteriorates hippocampal neurogenesis, which leads to memory impairment. Hesperidin (Hsd) is a plant-based bioflavonoid that can augment learning and memory. This study aimed to understand the effect of Hsd on the impairment of hippocampal neurogenesis and memory caused by VPA. The VPA (300 mg/kg) was administered by intraperitoneal injection twice daily for 14 days, and Hsd (100 mg/kg/day) was administered by oral gavage once a day for 21 days. All rats underwent memory evaluation using the novel object location (NOL) and novel object recognition (NOR) tests. Immunofluorescent staining of Ki-67, BrdU/NeuN, and doublecortin (DCX) was applied to determine hippocampal neurogenesis in cell proliferation, neuronal survival, and population of the immature neurons, respectively. VPA-treated rats showed memory impairments in both memory tests. These impairments resulted from VPA-induced decreases in the number of Ki-67-, BrdU/NeuN-, and DCX-positive cells in the hippocampus, leading to memory loss. Nevertheless, the behavioral expression in the co-administration group was improved. After receiving co-administration with VPA and Hsd, the numbers of Ki-67-, BrdU/NeuN-, and DCX-positive cells were improved to the normal levels. These findings suggest that Hsd can reduce the VPA-induced hippocampal neurogenesis down-regulation that results in memory impairments.

scholarly journals Protective effects of SGB121, ginsenoside F1-enriched ginseng extract, on scopolamine-induced cytotoxicity and memory impairments

2020 ◽  
Vol 74 ◽  
pp. 104165
Author(s):  
Tonking Bastola ◽  
Ramesh Pariyar ◽  
Byeong-Min Jeon ◽  
Jong-In Baek ◽  
Bo Yoon Chang ◽  
...  
Keyword(s):  
Protective Effects ◽  
Ginseng Extract ◽  
Memory Impairments

scholarly journals Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1407 ◽  
Author(s):  
You-Lin Tain ◽  
Julie Chan ◽  
Chien-Te Lee ◽  
Chien-Ning Hsu
Keyword(s):  
Methylation Status ◽  
Normal Diet ◽  
Male Offspring ◽  
Adult Offspring ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Male Adult ◽  
Methyl Donor ◽  
Adult Rat

Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2− level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet.

scholarly journals Protective Effects of 3-benzoyl-7-hydroxy Coumarin on Liver of Adult Rat Exposed to Aluminium Chloride

2021 ◽  
Vol 68 (1) ◽  
pp. 222-228
Author(s):  
Ahmet Özkaya ◽  
Kenan Türkan
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Aluminium Chloride ◽  
Control Group ◽  
Albino Rats ◽  
Activity Levels ◽  
Protective Effects ◽  
Adult Rat ◽  
Antioxidant Enzyme System ◽  
Hydroxy Coumarin

In this study, the effects of 3-benzoyl-7-hydroxy coumarin molecule on mineral and antioxidant enzymes were investigated in rat liver exposed to oxidative stress with aluminium chloride (AlCl3). Adult male Wistar albino rats were divided into four groups as Control, Coumarin, AlCl3, and Coumarin + AlCl3. Coumarin at the dose of 10 mg/kg and AlCl3 at the dose of 8.3 mg/kg were administered for 30 days every other day. In AlCl3 group, malondialdehyde (MDA), iron (Fe), aluminium (Al) and copper (Cu) levels increased compared to the control group, while glutathione (GSH) level, glutathione S-transferase (GST), and carboxylesterase (Ces) enzyme activity levels decreased. In Coumarin + AlCl3 group, MDA, Fe, Al and Cu levels decreased with the effect of coumarin compared to AlCl3 group, while GSH level, and GST enzyme activity levels increased. According to our results, AlCl3 generates oxidative stress in rat livers, and we believe that 3-benzoyl-7-hydroxy coumarin has an ameliorative effect on antioxidant enzyme system, Al, Fe and Cu levels.

scholarly journals Acute stress enhances adult rat hippocampal neurogenesis and activation of newborn neurons via secreted astrocytic FGF2

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Elizabeth D Kirby ◽  
Sandra E Muroy ◽  
Wayne G Sun ◽  
David Covarrubias ◽  
Megan J Leong ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Acute Stress ◽  
Memory Function ◽  
Brain Regions ◽  
Hippocampal Neurogenesis ◽  
Mammalian Brain ◽  
Stress Hormone ◽  
Adult Rat ◽  
Neural Stem Progenitor Cells ◽  
Newborn Neurons

Stress is a potent modulator of the mammalian brain. The highly conserved stress hormone response influences many brain regions, particularly the hippocampus, a region important for memory function. The effect of acute stress on the unique population of adult neural stem/progenitor cells (NPCs) that resides in the adult hippocampus is unclear. We found that acute stress increased hippocampal cell proliferation and astrocytic fibroblast growth factor 2 (FGF2) expression. The effect of acute stress occurred independent of basolateral amygdala neural input and was mimicked by treating isolated NPCs with conditioned media from corticosterone-treated primary astrocytes. Neutralization of FGF2 revealed that astrocyte-secreted FGF2 mediated stress-hormone-induced NPC proliferation. 2 weeks, but not 2 days, after acute stress, rats also showed enhanced fear extinction memory coincident with enhanced activation of newborn neurons. Our findings suggest a beneficial role for brief stress on the hippocampus and improve understanding of the adaptive capacity of the brain.

Protective effects of valproic acid on 6‐hydroxydopamine‐induced neuroinjury

2020 ◽  
Vol 35 (8) ◽  
pp. 840-848 ◽  
Author(s):  
Shih‐Wei Hsu ◽  
Pei‐Chen Hsu ◽  
Wen‐Shin Chang ◽  
Chien‐Chih Yu ◽  
Yun‐Chi Wang ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Protective Effects ◽  
6 Hydroxydopamine

The effects of soy on scopolamine-induced spatial learning and memory impairments are comparable to the effects of estradiol

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Narges Marefati ◽  
Amin Mokhtari-Zaer ◽  
Farimah Beheshti ◽  
Sareh Karimi ◽  
Zahra Mahdian ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Protective Effects ◽  
Memory Impairments ◽  
The Central Nervous System ◽  
Higher Doses

Abstract Background Modulatory effects of soy extract and estradiol on the central nervous system (CNS) have been reported. The effect of soy on scopolamine-induced spatial learning and memory in comparison to the effect of estradiol was investigated. Materials and methods Ovariectomized rats were divided into the following groups: (1) control, (2) scopolamine (Sco), (3) scopolamine-soy 20 (Sco-S 20), (4) scopolamine-soy 60 (Sco-S 60), (5) scopolamine-estradiol 20 (Sco-E 20) and (6) scopolamine-estradiol 60 (Sco-E 60). Soy extract, estradiol and vehicle were administered daily for 6 weeks before training in the Morris water maze (MWM) test. Scopolamine (2 mg/kg) was injected 30 min before training in the MWM test. Results In the MWM, the escape latency and traveled path to find the platform in the Sco group was prolonged compared to the control group (p < 0.001). Treatment by higher doses of soy improved performances of the rats in the MWM (p < 0.05 – p < 0.001). However, treatment with both doses of estradiol (20 and 60 μg/kg) resulted in a statistically significant improvement in the MWM (p < 0.01 – p < 0.001). Cortical, hippocampal and serum levels of malondialdehyde (MDA), as an index of lipid peroxidation, were increased which was prevented by soy extract and estradiol (p < 0.001). Cortical, hippocampal as well as serum levels of the total thiol, superoxide dismutase (SOD) and catalase (CAT) in Sco group were lower than the control group (p < 0.001) while they were enhanced when the animals were treated by soy extract and estradiol (p < 0.01 – p < 0.001). Conclusions It was observed that both soy extract and estradiol prevented learning and memory impairments induced by scopolamine in ovariectomized rats. These effects can be attributed to their protective effects on oxidative damage of the brain tissue.

scholarly journals Intranasal MSC-derived A1-exosomes ease inflammation, and prevent abnormal neurogenesis and memory dysfunction after status epilepticus

2017 ◽  
Vol 114 (17) ◽  
pp. E3536-E3545 ◽  
Author(s):  
Qianfa Long ◽  
Dinesh Upadhya ◽  
Bharathi Hattiangady ◽  
Dong-Ki Kim ◽  
Su Yeon An ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Memory Function ◽  
Hippocampal Neurogenesis ◽  
Medical Emergency ◽  
Memory Impairments ◽  
Functional Deficits ◽  
Persistent Inflammation ◽  
Antiepileptic Drug Treatment ◽  
Antiinflammatory Effects

Status epilepticus (SE), a medical emergency that is typically terminated through antiepileptic drug treatment, leads to hippocampus dysfunction typified by neurodegeneration, inflammation, altered neurogenesis, as well as cognitive and memory deficits. Here, we examined the effects of intranasal (IN) administration of extracellular vesicles (EVs) secreted from human bone marrow-derived mesenchymal stem cells (MSCs) on SE-induced adverse changes. The EVs used in this study are referred to as A1-exosomes because of their robust antiinflammatory properties. We subjected young mice to pilocarpine-induced SE for 2 h and then administered A1-exosomes or vehicle IN twice over 24 h. The A1-exosomes reached the hippocampus within 6 h of administration, and animals receiving them exhibited diminished loss of glutamatergic and GABAergic neurons and greatly reduced inflammation in the hippocampus. Moreover, the neuroprotective and antiinflammatory effects of A1-exosomes were coupled with long-term preservation of normal hippocampal neurogenesis and cognitive and memory function, in contrast to waned and abnormal neurogenesis, persistent inflammation, and functional deficits in animals receiving vehicle. These results provide evidence that IN administration of A1-exosomes is efficient for minimizing the adverse effects of SE in the hippocampus and preventing SE-induced cognitive and memory impairments.

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