scholarly journals Protective Effects ofBorago officinalisExtract on Amyloidβ-Peptide(25–35)-Induced Memory Impairment in Male Rats: A Behavioral Study

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Fatemeh Ghahremanitamadon ◽  
Siamak Shahidi ◽  
Somayeh Zargooshnia ◽  
Ali Nikkhah ◽  
Akram Ranjbar ◽  
...  
Keyword(s):  
Passive Avoidance ◽  
Memory Impairment ◽  
Neurodegenerative Disorder ◽  
Male Rats ◽  
Avoidance Task ◽  
Protective Effects ◽  
Frap Assay ◽  
Antioxidant Power ◽  
Borago Officinalis ◽  
Learning Impairment

Alzheimer’s disease (AD) is a neurodegenerative disorder and most common form of dementia that leads to memory impairment. In the present study we have examined the protective effects ofBorago officinalis(borage) extract on Amyloidβ(Aβ)-Induced memory impairment. Wistar male rats received intrahippocampal (IHP) injection of the Aβ(25–35) and borage extract throughout gestation (100 mg/kg). Learning and memory functions in the rats were examined by the passive avoidance and the Morris water maze (MWM) tasks. Finally, the antioxidant capacity of hippocampus was measured using ferric ion reducing antioxidant power (FRAP) assay. The results showed that Aβ(25–35) impaired step-through latency and time in dark compartment in passive avoidance task. In the MWM, Aβ(25–35) significantly increased escape latency and traveled distance. Borage administration attenuated the Aβ-induced memory impairment in both the passive avoidance and the MWM tasks. Aβinduced a remarkable decrease in antioxidant power (FRAP value) of hippocampus and borage prevented the decrease of the hippocampal antioxidant status. This data suggests that borage could improve the learning impairment and oxidative damage in the hippocampal tissue following Aβtreatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.

scholarly journals Butea superba Roxb. Extract Ameliorates Scopolamine-Induced Cognitive and Memory Impairment in Aged Male Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Kittipot Sirichaiwetchakoon ◽  
Sarawut Suksuphew ◽  
Rungrudee Srisawat ◽  
Griangsak Eumkeb
Keyword(s):  
Passive Avoidance ◽  
Memory Impairment ◽  
Neurodegenerative Disorder ◽  
Ex Vivo ◽  
Radical Scavenging ◽  
Male Rats ◽  
Passive Avoidance Test ◽  
Dependent Manner ◽  
Avoidance Test ◽  
Butea Superba

Butea superba Roxb. (B. superba) is a herb that has been used for rejuvenation, to improve sexual performance, or to prevent erectile dysfunction function. Alzheimer’s disease (AD) is a chronic neurodegenerative disorder that is the main cause of progressive dementia. This study aimed to investigate the amelioration for cognitive and memory dysfunction of B. superba ethanolic extract (BSE), a possible mechanism of action, and its toxicity. The results from the Y-maze test, novel object recognition test, and passive avoidance test exhibited that the administration of BSE at 50 mg/kg (BSL) and 200 mg/kg (BSH) could ameliorate scopolamine-induced cognitive impairment in all behavior testing. Moreover, BSE could prevent the cognitive deficit in a dose-dependent manner in a passive avoidance test. Furthermore, BSE inhibited acetylcholinesterase’s (AChE) ex vivo activity in the cerebral cortex and hippocampus. Also, the in vitro and ex vivo antioxidative effects of BSE revealed that BSE had free radical scavenging activities in both DPPH and FRAP assay. Furthermore, male rats treated with BSE at 200 mg/kg/day for two weeks could significantly increase serum testosterone compared with control ( P < 0.05 ). The GC-MS analysis and previous studies revealed that BSE contained propanoic acid, 3,3′-thiobis-, didodecyl ester, oleic acid, gamma-sitosterol, and stigmasterol which may play an important role in cognitive and memory impairment prevention. The toxicity test of BSE in rats at 50 and 200 mg/kg/day for two weeks showed that relative organ weight, serum creatinine, ALT, ALP, and CBC levels of both treated groups were not significantly different compared to the CON ( P > 0.05 ). These results suggest that BSE may not be toxic to the vital organ and blood. In conclusion, BSE has the potential to be developed as a health supplement product or medicine for AD prevention and treatment.

scholarly journals Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

2019 ◽  
Vol 20 (14) ◽  
pp. 3538 ◽  
Author(s):  
Eunjin Sohn ◽  
Hye-Sun Lim ◽  
Yu Jin Kim ◽  
Bu-Yeo Kim ◽  
Soo-Jin Jeong
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Passive Avoidance ◽  
Memory Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Acetylcholinesterase Activity ◽  
Hippocampal Neurogenesis ◽  
Avoidance Task ◽  
Y Maze

We explored the preventative effect of Annona atemoya leaf (AAL) extract on memory impairment in a scopolamine (SCO)-induced cognitive deficit mouse model. Fifty-eight mice were randomly divided into six groups and orally treated with AAL extract at (50, 100, or 200 mg/kg) or tacrine (TAC) for 21 days. Memory deficits were induced by a single injection of 1 mg/kg SCO (i.p.) and memory improvement was evaluated by using behavioral tests such as the passive avoidance task and Y-maze test. The levels of cholinergic functions, neuronal cell death, reactive oxygen species, and protein expression related to hippocampal neurogenesis were examined by immunohistochemical staining and western blotting. The administration of AAL extract improved memory impairment according to increased spontaneous alternation in the Y-maze and step-through latency in passive avoidance test. AAL extract treatment increased the acetylcholine content, choline acetyltransferase, and acetylcholinesterase activity in the hippocampus of SCO-stimulated mice. In addition, AAL extract attenuated oxidative stress-induced neuronal cell death of hippocampal tissue. In terms of the regulatory mechanisms, AAL extract treatment reversed the SCO-induced decreases in the expression of Akt, phosphorylation of cAMP response element binding protein, and brain-derived neurotrophic factor. Our findings demonstrate that AAL extract has the ability to alleviate memory impairment through preventative effect on cholinergic system dysfunction and oxidative stress-related neuronal cell death in a SCO-induced memory deficit animal model. Overall, AAL may be a promising plant resource for the managing memory dysfunction due to neurodegenerative diseases, such as Alzheimer’s disease (AD).

scholarly journals Renoprotective Effects of Origanum majorana Methanolic L and Carvacrol on Ischemia/Reperfusion-Induced Kidney Injury in Male Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Izadpanah Gheitasi ◽  
Arsalan Azizi ◽  
Navid Omidifar ◽  
Amir Hossein Doustimotlagh
Keyword(s):  
Vitamin E ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Protective Effects ◽  
Antioxidant Power ◽  
Antioxidant Parameters ◽  
Origanum Majorana

Background. The most important cause of acute renal failure in normal kidneys is ischemia-reperfusion (I/R) injury. The aim of the current study was to investigate the protective effects of Origanum majorana (OM) methanolic extract, carvacrol, and vitamin E on I/R-induced kidney injury in male rats. Material and Method. Thirty Wistar male rats were randomly allocated into 5 groups; sham, I/R, I/R + OM (300 mg/kg), I/R + carvacrol (75 mg/kg), and I/R + vitamin E (100 mg/kg). Renal function markers, oxidant-antioxidant parameters, and histopathological examination were evaluated. Results. It was exhibited that the urea, creatinine, protein carbonyl, glomerular filtration rate, total thiol, ferric reducing antioxidant power, and histopathological changes markedly reversed in the treatment groups with OM or carvacrol in comparison to the I/R merely group. Conclusion. We conclude that OM extract or its ingredient, carvacrol, exerts renoprotective impacts in I/R-induced kidney injury possibly by scavenging free radicals and increasing antioxidant power.

scholarly journals Cognitive-Enhancing Effect of Steamed and FermentedCodonopsis lanceolata: A Behavioral and Biochemical Study

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jin Bae Weon ◽  
Bo-Ra Yun ◽  
Jiwoo Lee ◽  
Min Rye Eom ◽  
Hyun-Jeong Ko ◽  
...  
Keyword(s):  
Passive Avoidance ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Ache Activity ◽  
Neurodegenerative Disorder ◽  
Biochemical Study ◽  
Bdnf Expression ◽  
Creb Phosphorylation ◽  
Avoidance Tests

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment.Codonopsis lanceolata(C. lanceolata) has been employed clinically for lung inflammatory diseases such as asthma, tonsillitis, and pharyngitis. The present study was undertaken to evaluate the effect of fermentedC. lanceolata(300, 500, and 800 mg/kg) on learning and memory impairment induced by scopolamine by using the Morris water maze and passive avoidance tests. To elucidate possible mechanism of cognitive-enhancing activity, we measured acetylcholinesterase (AchE) activity, brain-derived neurotrophic factor (BDNF), and cyclic AMP response element-binding protein (CREB) expression in the brain of mice. Administration of fermentedC. lanceolata(800 mg/kg) led to reduced scopolamine-induced memory impairment in the Morris water maze and passive avoidance tests. Accordingly, the administration of fermentedC. lanceolatainhibited AchE activity. Interestingly, the level of CREB phosphorylation and BDNF expression in hippocampal tissue of scopolamine-treated mice was significantly increased by the administration of fermentedC. lanceolata. These results indicate that fermentedC. lanceolatacan ameliorate scopolamine-induced memory deficits in mouse and may be an alternative agent for the treatment of AD.

scholarly journals NEUROPROTECTIVE EFFECT OF EPALRESTAT ON MEMORY IMPAIRMENT IN STREPTOZOTOCIN-INDUCED TYPE-2 DIABETIC RATS USING DIFFERENT BEHAVIORAL MODELS.

2018 ◽  
Vol 11 (1) ◽  
pp. 411 ◽  
Author(s):  
Shruti Jaiswal ◽  
Torgal Ss ◽  
Sanjay Mishra
Keyword(s):  
Passive Avoidance ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Potential Effect ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Protective Effects ◽  
Memory And Learning ◽  
Memory Enhancing

 Objective: The present study was designed to evaluate the protective effects of epalrestat (EPS) on memory and learning in type-2 diabetes.Methods: Sixty percent high-fat diet for 2 weeks and a single dose of streptozotocin (35 mg/kg, ip) was used to induce memory impairment in rats. Once the diabetes is confirmed, test drug (EPS - 13.5, 27, and 54 mg/kg, oral) and donepezil (1 mg/kg, oral) were administered to different groups of rats for 4 weeks followed by an assessment of memory and learning deficit using behavioral paradigms: Elevated plus maze (EPM), Morris water maze (MWM), and passive avoidance test.Results: EPS and donepezil showed significant improvement in learning and memory of rats, as indicated by markedly decreased escape latency to reach a hidden platform and increased time spent in target quadrant using MWM task, reduced transfer latency in EPM, and also there is a significant increase in the transfer latencies using passive avoidance test were noted. Memory-enhancing activity of EPS (13.5, 27, and 54 mg/kg) was comparable with the diabetic control group.Conclusion: The study findings suggest that memory-enhancing effect of EPS may be mediated by its antioxidant and anti-inflammatory activities. This recommends the potential effect of EPS therapy as a useful memory restorative agent in the treatment of neurodegenerative disease seen in type-2 diabetes rat.

NMDA receptors in the dorsal hippocampal area are involved in tramadol state-dependent memory of passive avoidance learning in mice

2018 ◽  
Vol 96 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Majid Jafari-Sabet ◽  
Hamed Mofidi ◽  
Mohammad-Sadegh Attarian-Khosroshahi
Keyword(s):  
Passive Avoidance ◽  
Memory Retrieval ◽  
Memory Impairment ◽  
Avoidance Task ◽  
Memory Retention ◽  
State Dependent ◽  
Dorsal Hippocampal ◽  
Opioid Receptor Agonist ◽  
Hippocampal Area ◽  
Μ Opioid Receptor

The precise neurobiological mechanisms of tramadol abuse underlying the cognitive function are still unknown. The aim of the present study was to examine the possible effects of intra-CA1 injections of N-methyl-d-aspartate (NMDA), a glutamate NMDA receptor (NMDAR) agonist, and d,l-2-amino-5-phosphonopentanoic acid (DL-AP5), a competitive NMDAR antagonist, on tramadol state-dependent memory. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice. Post-training i.p. administration of an atypical μ-opioid receptor agonist, tramadol (2.5 and 5 mg/kg), dose-dependently induced impairment of memory retention. Pre-test injection of tramadol (2.5 and 5 mg/kg) induced state-dependent retrieval of the memory acquired under post-training administration of tramadol (5 mg/kg) influence. Pre-test intra-CA1 injection of NMDA (10−5 and 10−4 μg/mouse) 5 min before the administration of tramadol (5 mg/kg, i.p.) dose-dependently inhibited tramadol state-dependent memory. Pre-test intra-CA1 injection of DL-AP5 (0.25 and 0.5 μg/mouse) reversed the memory impairment induced by post-training administration of tramadol (5 mg/kg). Pre-test administration of DL-AP5 (0.25 and 0.5 μg/mouse) with an ineffective dose of tramadol (1.25 mg/kg) restored the retrieval and induced tramadol state-dependent memory. It can be concluded that dorsal hippocampal NMDAR mechanisms play an important role in the modulation of tramadol state-dependent memory.

Nicotine-induced memory impairment by increasing brain oxidative stress

2009 ◽  
Vol 4 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Lucian Gorgan
Keyword(s):  
Oxidative Stress ◽  
Passive Avoidance ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Memory Performance ◽  
Long Term Memory ◽  
Avoidance Task ◽  
Term Memory ◽  
Y Maze ◽  
Brain Oxidative Stress

AbstractMale Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.

scholarly journals NEUROPROTECTIVE EFFECT OF EPALRESTAT ON MEMORY IMPAIRMENT IN STREPTOZOTOCIN-INDUCED TYPE-2 DIABETIC RATS USING DIFFERENT BEHAVIORAL MODELS.

2018 ◽  
Vol 11 (1) ◽  
pp. 411
Author(s):  
Shruti Jaiswal ◽  
Torgal Ss ◽  
Sanjay Mishra
Keyword(s):  
Passive Avoidance ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Potential Effect ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Protective Effects ◽  
Memory And Learning ◽  
Memory Enhancing

 Objective: The present study was designed to evaluate the protective effects of epalrestat (EPS) on memory and learning in type-2 diabetes.Methods: Sixty percent high-fat diet for 2 weeks and a single dose of streptozotocin (35 mg/kg, ip) was used to induce memory impairment in rats. Once the diabetes is confirmed, test drug (EPS - 13.5, 27, and 54 mg/kg, oral) and donepezil (1 mg/kg, oral) were administered to different groups of rats for 4 weeks followed by an assessment of memory and learning deficit using behavioral paradigms: Elevated plus maze (EPM), Morris water maze (MWM), and passive avoidance test.Results: EPS and donepezil showed significant improvement in learning and memory of rats, as indicated by markedly decreased escape latency to reach a hidden platform and increased time spent in target quadrant using MWM task, reduced transfer latency in EPM, and also there is a significant increase in the transfer latencies using passive avoidance test were noted. Memory-enhancing activity of EPS (13.5, 27, and 54 mg/kg) was comparable with the diabetic control group.Conclusion: The study findings suggest that memory-enhancing effect of EPS may be mediated by its antioxidant and anti-inflammatory activities. This recommends the potential effect of EPS therapy as a useful memory restorative agent in the treatment of neurodegenerative disease seen in type-2 diabetes rat.

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