scholarly journals Memory-Enhancing Effects of Mangosteen Pericarp Water Extract through Antioxidative Neuroprotection and Anti-Apoptotic Action

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 34
Author(s):  
Yeonsoo Oh ◽  
Ha Thi Thu Do ◽  
Sunyoung Kim ◽  
Young-Mi Kim ◽  
Young-Won Chin ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Caspase 3 ◽  
Water Extract ◽  
Antioxidant Property ◽  
Morris Water Maze Test ◽  
Oxygen Species ◽  
Cortical Cells ◽  
Maze Test ◽  
Pharmacological Potential ◽  
Memory Enhancing

Mangosteen has long been utilized as a traditional medicine in Southeast Asia. Diverse extracts of mangosteen pericarp and its bioactive xanthones exhibit various bioactivities. However, the pharmacological potential of mangosteen pericarp water extract (MPW) has not been reported yet. This study used primary cultured rat cortical cells to investigate the effect of MPW on neurotoxicity. We found that MPW inhibited neurotoxicity and production of reactive oxygen species triggered by Aβ(25–35) or excitatory amino acids. MPW inhibited caspase 3 activation and DNA fragmentation in Aβ(25–35)- or N-methyl-D-aspartate-treated cells, suggesting an anti-apoptotic action. Additionally, MPW reduced lipid peroxidation and scavenged 1,1-diphenyl-2-picrylhydrazyl radicals, assuring its antioxidant property. Furthermore, MPW suppressed β-secretase and acetylcholinesterase activities. These findings prompted us to evaluate its effect on memory dysfunction in scopolamine-treated mice using Morris water maze test. Oral administration of MPW at the dosage of 50, 100, or 300 mg/kg for four days significantly decreased the latency time to find the platform and markedly increased the swimming time in the target quadrant. Taken together, our results suggest that MPW exerts memory-enhancing effect through antioxidative neuroprotection and anti-apoptotic action. Accordingly, MPW may have a potential to prevent or treat memory impairment associated with Alzheimer’s disease.

Soybean Isoflavones Influences Learning and Memory and Caspase-3 Levels in the Hippocampus of Rats after MWM Test

2013 ◽  
Vol 411-414 ◽  
pp. 3178-3180
Author(s):  
Li Hai Jin ◽  
Xing Yu Zhao ◽  
Wei Zhang ◽  
Wei Chen ◽  
Guo Qing Sun ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Caspase 3 ◽  
Morris Water Maze Test ◽  
Once Daily ◽  
Soybean Isoflavones ◽  
Maze Test ◽  
Intermediate Dose

We assessed the effectiveness and mechanism of action of Soybean Isoflavones on learning and memory and Caspase-3 levels in the hippocampus of rats after Morris water maze (MWM test). Soybean Isoflavones (200,400 or 800 mg/kg/d) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of Soybean Isoflavones to increase learning and memory impairment. The levels of Caspase-3 in hippocampus of rats were detected by Westernblot after MWM test. Compared to untreated controls (P<0.01), MWM could be prolonged after Soybean Isoflavones treatment (P<0.05 for="" low="" and="" intermediate="" dose="" groups="" westernblot="" analysis="" showed="" that="" the="" protein="" expression="" of="" caspase-3="" was="" decreased="" in="" different="" concentration="" soybean="" isoflavones="" i="">P<0.05 and="" i="">P<0.01, respectively). The results suggest that Soybean Isoflavones is effective in improving the learning and memory in rats , the mechanism of which may be related Caspase ways.

scholarly journals Effect of Evodia rutaecarpa (Juss) Benth extract on Alzheimer disease in mice

2020 ◽  
Vol 19 (4) ◽  
pp. 823-828
Author(s):  
Ang Cai ◽  
Liu Xiao ◽  
Yan-Ping Zhou ◽  
Zhi-Guo Zhang ◽  
Quan-Wei Yang
Keyword(s):  
Cognitive Function ◽  
Alzheimer Disease ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Evodia Rutaecarpa ◽  
Mouse Hippocampus

Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in the animals treated with 400 mg/kg ERBE (20.5 ± 1.3 s) was significantly higher than untreated 3xTg-AD mice (12.4 ± 1.3 s, p < 0.01). In addition, ERBE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.4 ± 0.2, p < 0.05) and TrkB (1.1 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: The results suggest that ERBE administration may be a useful strategy for treating memory impairment induced by several neurodegenerative diseases. Keywords: Evodia rutaecarpa, Alzheimer, Memory impairment, NeuN-positive cells

scholarly journals Xanthoceraside Ameliorates Mitochondrial Dysfunction Contributing to the Improvement of Learning and Memory Impairment in Mice with Intracerebroventricular Injection of Aβ1-42

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Xue-Fei Ji ◽  
Tian-Yan Chi ◽  
Qian Xu ◽  
Xiao-Lu He ◽  
Xiao-Yu Zhou ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Mitochondrial Respiratory Chain ◽  
Morris Water Maze Test ◽  
Mice Model ◽  
Maze Test ◽  
Y Maze ◽  
Abnormal Increase ◽  
Improved Learning

The effects of xanthoceraside on learning and memory impairment were investigated and the possible mechanism associated with the protection of mitochondria was also preliminarily explored in Alzheimer’s disease (AD) mice model induced by intracerebroventricular (i.c.v.) injection of Aβ1-42. The results indicated that xanthoceraside (0.08–0.32 mg/kg) significantly improved learning and memory impairment in Morris water maze test and Y-maze test. Xanthoceraside significantly reversed the aberrant decrease of ATP levels and attenuated the abnormal increase of ROS levels both in the cerebral cortex and hippocampus in mice injected with Aβ1-42. Moreover, xanthoceraside dose dependently reversed the decrease of COX, PDHC, and KGDHC activity in isolated cerebral cortex mitochondria of the mice compared with Aβ1-42 injected model mice. In conclusion, xanthoceraside could improve learning and memory impairment, promote the function of mitochondria, decrease the production of ROS, and inhibit oxidative stress. The improvement effects on mitochondria may be through withstanding the damage of Aβto mitochondrial respiratory chain and the key enzymes in Kreb’s cycle. Therefore, the results from present study and previous study indicate that xanthoceraside could be a competitive candidate for the treatment of AD.

scholarly journals Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice

2021 ◽  
Vol 18 (9) ◽  
pp. 1903-1907
Author(s):  
Cen Su ◽  
Ping Niu ◽  
Yao-ming Xu ◽  
Ye Feng ◽  
Hai-ping Xia
Keyword(s):  
Cognitive Function ◽  
Protective Effect ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Immunohistochemical Assay ◽  
Maze Test ◽  
Acorus Tatarinowii

Purpose: To investigate the protective effect of Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice. Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in animals treated with 600 mg/kg ATE (24.8 ± 1.3 s) was significantly increased relative to ontreated 3xTg-AD mice (8.5 ± 1.0 s, p < 0.01). In addition, ATE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF (1.9 ± 0.4, p < 0.05) and TrkB (1.9 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: These results suggest that ATE treatment may be a useful strategy for managing memory impairment induced by several neurodegenerative diseases.

Pecan Oil Influences Learning and Memory and NF-κB Levels in the Hippocampus of Rats after MWM Test

2014 ◽  
Vol 912-914 ◽  
pp. 1957-1960
Author(s):  
Ying Li ◽  
Xing Yu Zhao ◽  
Xue Lian Jin ◽  
Guo Qing Sun ◽  
Song Liu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Mechanism Of Action ◽  
Water Maze ◽  
Memory Impairment ◽  
Morris Water Maze Test ◽  
Once Daily ◽  
Maze Test ◽  
Intermediate Dose

We assessed the effectiveness and mechanism of action of Pecan oil on learning and memory and NF-κB levels in the hippocampus of rats after Morris water maze (MWM test). Pecan oil (200,400 or 800 mg/kg/d) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of Pecan oil to increase learning and memory impairment. The levels of NF-κB in hippocampus of rats were detected by Westernblot after MWM test. Compared to untreated controls (P<0.01), MWM could be prolonged after Pecan oil treatment (P<0.05 for low and intermediate dose groups). Westernblot analysis showed that the protein expression of NF-κB was decreased in different concentration Pecan oil(P<0.05 and P<0.01, respectively). The results suggest that Pecan oil is effective in improving the learning and memory in rats, the mechanism of which may be related NF-κB expression decreasing.

scholarly journals Biochanin A Attenuates Ovariectomy-Induced Cognition Deficit via Antioxidant Effects in Female Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Yanmeng Zhou ◽  
Bingbing Xu ◽  
Haiyang Yu ◽  
Wei Zhao ◽  
Xinxin Song ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Hippocampal Neurons ◽  
Water Maze ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Primary Cultures ◽  
Biochanin A ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Ovx Rats

Background: Impairment of memory and cognition is one of the major symptoms in women with postmenopausal disorders due to estrogen deficiency, which accounts for the much higher prevalence of Alzheimer’s disease in females. Biochanin A (BCA), a natural phytoestrogen, has been reported to protect neurons against ischemic brain injury. However, the neuroprotective effects of BCA in the postmenopausal-like model of ovariectomized (OVX) rats remain to be investigated.Methods: All the rats except for the sham group underwent the resection of bilateral ovaries. Seven days after the OVX surgery, rats were randomly divided into six groups: sham, OVX, OVX + BCA (5 mg/kg), OVX + BCA (20 mg/kg), OVX + BCA (60 mg/kg), and OVX + estradiol (E2; 0.35 mg/kg), which were administrated daily by gavage for 12 weeks. Learning and memory were examined using the Morris water-maze test before the end of the experiment. Morphological changes of the rat hippocampus were observed by HE staining and electron microscopy. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in the hippocampus were measured. The effect of BCA on cell viability was measured in the presence of hydrogen peroxide (H2O2) using CCK8. Flow cytometry was used to measure neuronal apoptosis and reactive oxygen species (ROS) induced by H2O2. Expression of Bcl-2, Bax, and Caspase-3 was determined by Western blotting using hippocampal tissues and primary cultures of hippocampal neurons.Results: Chronic treatment with BCA mimicked the ability of E2 to reverse the deficit of learning and memory in the Morris water-maze test in OVX rats. BCA normalized OVX-induced morphological changes as revealed by HE staining and electron microscopy. In addition, BCA significantly decreased the levels of MDA, the biomarker of oxidative damage, and increased the activity of the intracellular antioxidant enzymes SOD and GSH-Px in OVX rats. Further, in primary cultures of hippocampal neurons, BCA reversed H2O2-induced decreases in cell viability and accumulation of ROS. Finally, BCA reversed OVX- or H2O2-induced increases in Bax and Caspase-3 and decreases in Bcl-2 in the hippocampus and primary cultures of hippocampal neurons.Conclusion: These results suggest that BCA improves memory through its neuroprotective properties in the brain under the circumstance of estrogen deficiency and can be used for treatment of memory loss in postmenopausal women.

scholarly journals EVALUATION OF MEMORY-ENHANCING ACTIVITY FOR ERYTHRININE FROM LEAF EXTRACT OF ERYTHRINA INDICA

2019 ◽  
pp. 101-103
Author(s):  
KAMALRAJ R ◽  
SUBHASHREE G R
Keyword(s):  
Normal Saline ◽  
Water Maze ◽  
Leaf Extract ◽  
Positive Control ◽  
Negative Control ◽  
Test Method ◽  
Morris Water Maze Test ◽  
Memory Enhancement ◽  
Maze Test ◽  
Memory Enhancing

Objective: The objective of the study was to investigate the memory-enhancing activity for erythrinine (ring-c-oxygenated Erythrina alkaloid) from leaf extract of Erythrina indica in mice. Methods: The study protocol designed in the way that it was carried out for 21 successive days by administrating the 5 mg/kg, s.c doses of isolated erythrinine to mice and the profile was challenged against the mice feeds with normal saline as a positive control and the mice treated with 5 mg/kg, s.c corticosterone as a negative control for the amnesia using Morris water maze test method. Results: Erythrinine-administered mice are showing remarkable retention of the memory (9.07±0.52) on the 21st day as such of the positive control normal saline (10.14±0.22) and against the negative control corticosterone-injected mice (70.86±0.54). Conclusions: The dose of 5 mg/kg s.c of isolated erythrinine from the leaf of E. indica shows the remarkable memory enhancement when it was investigated with the memory weakening induced test by corticosterone in mice’s using 5 mg/kg s.c. However, further studies required to elucidate the exact mechanism of action for developing its as potent memory-enhancing drug.

Abstract TP446: Rosuvastatin Improves Cerebral Hemodynamics in Rats With Chronic Cerebral Hypoperfusion

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Xiaomei Xie ◽  
Kangping Song ◽  
Li'an Huang
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Morris Water Maze ◽  
Water Maze ◽  
Caspase 3 ◽  
Treated Group ◽  
Cerebral Hypoperfusion ◽  
Morris Water Maze Test ◽  
Vehicle Group ◽  
Maze Test

Objective: Chronic cerebral hypoperfusion (CCH) is a common consequence of various cerebral vascular disorders, hemodynamics and blood composition changes, which can lead to neurodegenerative injury and cognitive dysfunction. Therefore, it is important to take measures to prevent or reverse its development. Methods: Eighty Sprague-Dawley rats were randomly divided into five groups: Sham group, Vehicle groups (2-week group and 4-week group), Rosuvastatin-treated groups (2-week group and 4-week group). Both vehicle and treated group rats were treated with bilateral common carotid artery occlusion (BCCAO). Then rats in the treated group were intravenously injection with rosuvastatin (0.2 mg/kg/day) daily for 14 days beginning 24 hours after BCCAO. The vehicle groups were given the same amount of saline. The MRI ASL technique was used to scan cerebral blood flow (CBF) at pre-occlusion, BCCAO, 1, 2, 3, and 4 weeks after operation. Morris water maze test detected spatial memory abilities of the treated and vehicle rats after BCCAO. Immunofluorescence staining was used to detect the expression of CD34, GFAP, NeuN and Caspase-3 positive cells in hippocampus. Results: CBF decreased significantly after BCCAO in both rosuvastatin-treated and vehicle groups and then increased gradually. The CBF of the treated group was basically recovered to baseline levels at 1 or 2 weeks after BCCAO. But it took the vehicle group 4 weeks to restore to baseline. The vertebral artery (VA) diameter of the treated group was greater than that of the vehicle group (p<0.05), and the recovery of CBF and the dilation of VA were more evident during the administration period. Similarly, the escape latency of the treated group rats was also less than the vehicle group in Morris Water Maze test. In addition, the number of CD34 + and NeuN + cells in the hippocampus of the treated group was more than that in the vehicle group (p<0.01), while the number of GFAP + and Caspase-3 + cells was less than in the vehicle group (p<0.01). Conclusion: Rosuvastatin can accelerate the recovery of cerebral blood flow in CCH rats, which may be related to the dilation of VAs and angiogenesis; and its effects on reducing astrocyte activation and neuroprotection may help to ameliorate cognitive dysfunction in CCH rats.

Ropivacaine Protects against Memory Impairment and Hippocampal Damage in a Rat Neurodegeneration Model

Pharmacology ◽  
2018 ◽  
Vol 102 (5-6) ◽  
pp. 307-315 ◽  
Author(s):  
Kuan-Ming Chiu ◽  
Tzu-Yu Lin ◽  
Ming-Yi Lee ◽  
Cheng-Wei Lu ◽  
Ming-Jiuh Wang ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Memory Impairment ◽  
Caspase 3 ◽  
Glutamate Release ◽  
Glutamate Excitotoxicity ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Morris Water Maze Test ◽  
Tunel Staining ◽  
Hippocampal Damage ◽  
Fluoro Jade B

Background: Ropivacaine, a long-acting amide local anesthetic agent, has been demonstrated to inhibit glutamatergic transmission. Glutamate neurotoxicity plays a pivotal role in the pathogenesis of brain disorders. The purpose of this study is to investigate the neuroprotective effect of ropivacaine against brain damage induced by kainic acid (KA), an analogue of glutamate. Methods: Rats were injected with ropivacaine (0.4 or 2 mg/kg, intraperitoneal) 30 min before KA treatment (15 mg/kg, intraperitoneal). KA-induced memory impairment was evaluated using the Morris water maze test. Extracellular hippocampal glutamate levels were assessed using high-performance liquid chromatography. Neuronal death was verified using Fluoro-Jade B and neutral red staining, and apoptosis was determined through terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Western blotting was conducted to assay the levels of activated (cleaved) caspase-3 and the phosphorylation of different mitogen-activated protein kinases (MAPKs). ­Results: Ropivacaine pretreatment effectively prevented KA-induced memory impairment. KA-induced elevations of ­glutamate release in rat hippocampi were inhibited by pretreatment with ropivacaine. Histopathological and TUNEL staining analyzes showed that ropivacaine inhibited KA-induced neuronal death and apoptosis in the hippocampal CA3 region. KA-induced caspase-3 activation and MAPKs phosphorylation in the hippocampus were also reduced by ropivacaine pretreatment. Conclusions: This study ­demonstrates that ropivacaine executes a protective action against KA-induced neuronal damage and apoptosis in vivo. Protective effects may be caused by glutamate level reduction, caspase-3 activation suppression, and MAPKs phosphorylation reduction. Our findings indicate that ropivacaine can benefit prevention or treatment of glutamate excitotoxicity-related neurodegenerative diseases.

Sign in / Sign up

Export Citation Format

Share Document