Panax Notoginseng Burk Attenuates Impairment of Learning and Memory Functions and Increases ED1, BDNF and β-Secretase Immunoreactive Cells in Chronic Stage Ischemia-Reperfusion Injured Rats

2008 ◽  
Vol 36 (04) ◽  
pp. 685-693 ◽  
Author(s):  
Chin-Min Chuang ◽  
Ching-Liang Hsieh ◽  
Hui-Yi Lin ◽  
Jaung-Geng Lin
Keyword(s):  
Cerebral Infarction ◽  
Learning And Memory ◽  
Radial Maze ◽  
Ischemia Reperfusion ◽  
Panax Notoginseng ◽  
Cerebral Infarct ◽  
Control Group ◽  
Memory Functions ◽  
Activated Microglia ◽  
Maze Test

Panax Notoginseng Burk (PN) has been reported to improve blood circulation, as well as learning and memory functions. The purpose of the present study was to investigate the effect of PN on learning and memory functions in chronic cerebral infarct rats. A cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and right middle cerebral artery for 90 min followed by reperfusion for 4 weeks. PN (0.5 g/kg) was administered orally 3 days per week for 4 weeks, whereas the control group provided bait and water only. The learning and memory functions were estimated by measuring how successful rats were able to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed. The brains were sectioned and analyzed for ED1, glial fibrillary acid protein (GFAP), nuclear factor-κB, and brain derivative neurotrophin factor (BDNF) and β-secretase by immunostaining. Cerebral infarct rats given PN were able to successfully navigate the 8-arm radial maze test four weeks after cerebral infarction. PN also increased ED1, BDNF and β-secretase immunoreactive cells, but did not increase GFAP and NF-κB immunoreactive cells. PN attenuated the reduction in learning and memory functions induced by cerebral infarction in cerebral ischemia-reperfusion injured rats; it also increased the amount of activated microglia and BDNF. These data suggest that the effect of PN, at least in part, is closely related to the increase in BDNF that was generated by activated microglia. The effect that PN has on astrocytes, NF-κB and β-secreatase immunoreactive cells requires further study.

scholarly journals Minocycline improves learning and memory functions in ischemic stroke rats via reduction of cerebral ischemia-induced neuroinflammation and apoptosis

2022 ◽  
Vol 20 (2) ◽  
pp. 287-292
Author(s):  
Li Li ◽  
Xiaolian Xing ◽  
Qian Li ◽  
Qinqin Zhang ◽  
Lu Fu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Protein Expression ◽  
Learning And Memory ◽  
Cell Apoptosis ◽  
Expression Level ◽  
Control Group ◽  
Volume Number ◽  
Memory Functions

Purpose: To study the effect minocycline on learning and memory functions in ischemic stroke rats, and the underlying mechanism. Methods: 60 adult male SD rats were randomly divided into control group, ischemic brain damage (6 and 24 h MACO) groups; and 6 and 24 h minocycline groups, with 12 rats in each group. The volume of cerebral infarction, neuronal cell apoptosis, NF-κB protein expression, learning and memory ability, and the number of Iba-1+CD206-positive cells, and CD206/CD68 mRNA expressions in sham group, 6 h MACO group and 6 h minocycline group were determined and compared. Results: The number of iba-1 +CD206-positive cells, expression level of CD206 mRNA, frequency of platform crossing, and percentage of third quadrant route in 6 h minocycline group were significantly higher than the corresponding values in 6 h MACO group. However, the cerebral infarction volume, number of Nini-positive cells, and the NF- B protein expression levels were markedly reduced, relative to corresponding values in 6 h MACO rats. The number of iba-1+CD206-positive cells was significantly lower in 6 h MACO rats than in sham rats, while the expression level of CD68 mRNA was significantly higher (p < 0.05). The number of TUNEL-positive cells in 6 and 24 h minocycline groups were markedly lower than that in 6 h MACO group (p < 0.05). Conclusion: Minocycline improves learning and memory of ischemic stroke rats by relieving the neuroinflammation induced by cerebral ischemia and cell apoptosis. Thus, the compound can be further developed for management learning and memory deficits in stroke patients.

scholarly journals Glutathione Suppresses Cerebral Infarct Volume and Cell Death after Ischemic Injury: Involvement of FOXO3 Inactivation and Bcl2 Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juhyun Song ◽  
Joohyun Park ◽  
Yumi Oh ◽  
Jong Eun Lee
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Cerebral Infarction ◽  
Infarct Size ◽  
Cell Survival ◽  
Ischemia Reperfusion ◽  
Ischemic Injury ◽  
Cerebral Infarct ◽  
Ros Scavenging ◽  
The Brain

Ischemic stroke interrupts the flow of blood to the brain and subsequently results in cerebral infarction and neuronal cell death, leading to severe pathophysiology. Glutathione (GSH) is an antioxidant with cellular protective functions, including reactive oxygen species (ROS) scavenging in the brain. In addition, GSH is involved in various cellular survival pathways in response to oxidative stress. In the present study, we examined whether GSH reduces cerebral infarct size after middle cerebral artery occlusionin vivoand the signaling mechanisms involved in the promotion of cell survival after GSH treatment under ischemia/reperfusion conditionsin vitro. To determine whether GSH reduces the extent of cerebral infarction, cell death after ischemia, and reperfusion injury, we measured infarct size in ischemic brain tissue and the expression of claudin-5 associated with brain infarct formation. We also examined activation of the PI3K/Akt pathway, inactivation of FOXO3, and expression of Bcl2 to assess the role of GSH in promoting cell survival in response to ischemic injury. Based on our results, we suggest that GSH might improve the pathogenesis of ischemic stroke by attenuating cerebral infarction and cell death.

scholarly journals Glutamate Elicits Therapeutic Responses in Light-Induced Sleep-Deprived Zebrafish, Danio rerio

2021 ◽  
Vol 14 (4) ◽  
pp. 1577-1583
Author(s):  
Uthirakumar Devaraj
Keyword(s):  
Sleep Deprivation ◽  
Learning And Memory ◽  
Major Effect ◽  
Control Group ◽  
The Novel ◽  
Behavioural Changes ◽  
Psychiatric Illnesses ◽  
Maze Test ◽  
Spectrofluorimetric Method ◽  
Tank Test

Sleep deprivation disrupts most neurotransmitters, which can lead to adverse behavioural changes and other psychiatric illnesses. Many neurotransmitter systems, including dopamine (DA), serotonin (5-HT), norepinephrine (N.E.) and GABA, have been implicated in the pathophysiology of mood disorders. The precise significance of sleep deprivation (S.D.) changes in the neurotransmitter levels and the mechanism underlying behavioural alterations is unknown. According to research, sleep deprivation (S.D.) has a major effect on an individual’s quality of life and ability to perform essential physiological functions. As a result, we wanted to confirm the levels of neurotransmitters and behavioural modifications in zebrafish after 24, 48, and 72 hours of sleep deprivation and glutamate treatment on the sleep-deprived groups. The T-maze test was used to assess learning and memory alterations in zebrafish. We used the Novel Tank Test (NTT) and Light and Dark Test (LDT) to examine the anxiety-like behaviour. The spectrofluorimetric method was used to determine the quantities of DA, 5-HT, N.E. and GABA. From this study, it is evident that 72h sleep-deprived fish had a loss of learning and memory via T-maze test and also the anxiety levels were very high in the sleep-deprived group than the other groups. The groups that received glutamate after sleep deprivation showed betterment in the behavioural response. Also, the levels of neurotransmitters were increased in the glutamate treated groups than the sleep-deprived groups. Our findings indicate that sleep loss dramatically impairs behavioural responses and disrupts most neurotransmitter concentrations. When sleep-deprived fish were given glutamate, their behaviour and neurotransmitter levels were nearly identical to those of the control group. This study will have a greater impact on sleep deprivation therapy and pave the way for using the neurotransmitters as external therapeutic agents in treating sleep deprivation and other behavioural changes related to sleep deprivation.It has been suggested that zebrafish is an excellent testing subject for loss of sleep on cognition and that it may also be an efficient model for unravelling the pathways that underpin learning and memory formation.

The Anti-Inflammatory Effect of Paeoniflorin on Cerebral Infarction Induced by Ischemia-Reperfusion Injury in Sprague-Dawley Rats

2010 ◽  
Vol 38 (01) ◽  
pp. 51-64 ◽  
Author(s):  
Nou-Ying Tang ◽  
Chung-Hsiang Liu ◽  
Ching-Tou Hsieh ◽  
Ching-Liang Hsieh
Keyword(s):  
Cerebral Infarction ◽  
Neurological Deficit ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Area ◽  
Cerebral Infarct ◽  
Apoptotic Cells ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pre Treatment

Paeoniflorin, a component in Paeonia lactiflora Pall, inhibits nuclear factor-κB expression in chronic hypoperfusion rat and has anti-inflammatory properties. Therefore, the aim of the present study was to investigate the effect of paeoniflorin on cerebral infarct, and the involvement of anti-inflammation. We established an animal model of cerebral infarct by occluding both the common carotid arteries and the right middle cerebral artery for 90 min, followed by reperfusion of 24 hours. The ratios of cerebral infarction area to total brain area, and neuro-deficit score were used as an index to observe the effects of paeoniflorin on cerebral infarct. ED1 (mouse anti rat CD68), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), intercellular adhesion molecular-1 (ICAM-1), myeloperoxidase (MPO) immunostaining and apoptotic cells in the cerebral infarction region also were studied. The results indicated that both pre-treatment and post-treatment with paeoniflorin reduced the ratio of cerebral infarction area; pre-treatment with paeoniflorin also reduced the neurological deficit score. The counts of ED1, IL-1β, TNF-α, ICAM-1 of microvessels and MPO immunoreactive cells and apoptotic cells were increased in the cerebral infarction region; however, these increases were reduced by Paeoniflorin pre-treatment. In conclusion, Paeoniflorin reduced cerebral infarct and neurological deficit in ischemia-reperfusion injured rats, suggesting that paeoniflorin may have a similar effect in humans and might be a suitable treatment for stroke. Paeoniflorin reduced cerebral infarct, at least in part, involves the anti-inflammatory properties.

scholarly journals Neuroprotective Effect of Paeonol Mediates Anti-Inflammation via Suppressing Toll-Like Receptor 2 and Toll-Like Receptor 4 Signaling Pathways in Cerebral Ischemia-Reperfusion Injured Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Wen-Yen Liao ◽  
Tung-Hu Tsai ◽  
Tin-Yun Ho ◽  
Yi-Wen Lin ◽  
Chin-Yi Cheng ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Signaling Pathways ◽  
Ischemia Reperfusion ◽  
Neurological Deficits ◽  
Control Group ◽  
Toll Like Receptor ◽  
Cerebral Ischemia Reperfusion ◽  
Infarction Volume ◽  
Anti Inflammatory

Paeonol is a phenolic compound derived fromPaeonia suffruticosaAndrews (MC) andP. lactifloraPall (PL). Paeonol can reduce cerebral infarction volume and improve neurological deficits through antioxidative and anti-inflammatory effects. However, the anti-inflammatory pathway of paeonol remains unclear. This study investigated the relationship between anti-inflammatory responses of paeonol and signaling pathways of TLR2 and TLR4 in cerebral infarct. We established the cerebral ischemia-reperfusion model in Sprague Dawley rats by occluding right middle cerebral artery for 60 min, followed by reperfusion for 24 h. The neurological deficit score was examined, and the brains of the rats were removed for cerebral infarction volume and immunohistochemistry (IHC) analysis. The infarction volume and neurological deficits were lower in the paeonol group (pretreatment with paeonol; 20 mg/kg i.p.) than in the control group (without paeonol treatment). The IHC analysis revealed that the number of TLR2-, TLR4-, Iba1-, NF-κB- (P50-), and IL-1β-immunoreactive cells and TUNEL-positive cells was significantly lower in the paeonol group; however, the number of TNF-α-immunoreactive cells did not differ between the paeonol and control groups. The paeonol reveals some neuroprotective effects in the model of ischemia, which could be due to the reduction of many proinflammatory receptors/mediators, although the mechanisms are not clear.

scholarly journals Impact of amitriptyline on learning and memory

2021 ◽  
Vol 5 (1) ◽  
pp. 009-015
Author(s):  
CC Mfem ◽  
SA Seriki
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Acquisition Trial ◽  
Water Maze ◽  
Treated Group ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Maze Test ◽  
Significant Difference ◽  
Retention Trial

Background/aim: Amitriptyline belongs to class of known as tricycline antidepresant (TCA) that is being used to treat anxiety and depressive states. It may help improve mood and feelings of well-being, relieve anxiety and tension, help to improve sleep and increase energy level. The study investigated the effect of amitriptyline on learning and memory using eighteen (18) healthy Swiss mice of both sexes weighing 16 – 25 g. Method: The animals were divided into three (3) groups consisting of six (6) animals each. Group 1 served as the control group, Group 2 was administered with amitriptyline at a dose of 3 mg/kg body weight dissolved in 3 mls of distilled water, and used to test for learning, while Group three was also given similar administration like Group 2, but used to test for memory. All the animals were tested for learning and memory performance using Novel object recognition task and Morris water maze test. Results: The results obtained from the Novel object recognition task showed that there was a significant decrease (p < 0.05) in total object approach in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant decrease (p < 0.05) in retention trial of amitriptyline group when compared to retention trial in the control group. There was a significant decrease (p < 0.05) in total duration exploring objects in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant increase (p < 0.05) in total duration exploring objects in retention trial of amitriptyline treated group when compared to the retention trial of the control group. There was a significant decrease (p < 0.05) in the index of habituation of amitriptyline treated group when compared to the control group. The index of discrimination showed a significant increase (p < 0.05) in amitriptyline treated group when compared to the control group and a significant decrease (p < 0.05) in amitriptyline group when compared to the control group. In the Morris water maze test, Day 1 – 3 were for acquisition training, day 4 – 6 reversal training, day 7 the probe trial day and day 8 the visible platform day. During acquisition training in the Morris water maze test, there was no significant difference in Swim latencies in day 1 and 2. However in day 3, there was a significant increase (p < 0.05) in swim latency of group compared to control group and a significant decrease (p < 0.05) in swim latency of amitriptyline treated group compared to the control group. During reversal training in day 1, 2 and 3, there was no significant difference in swim latency among the three groups. Results for the retention quadrant in the probe trials showed a significant decrease (p < 0.01) in amitriptyline group when compared to the control group. Conclusion: Results suggest that amitriptyline impairs learning and memory functions.

Improvement of Impaired Memory in Mice by Schisandrin

2013 ◽  
Vol 750-752 ◽  
pp. 1533-1538
Author(s):  
Yan Chun Wang ◽  
Kuang Ren ◽  
Nan Shen ◽  
Xiao Dong Huang ◽  
Hong Yan Fan
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Cellular Response ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Tissue Samples ◽  
Pentobarbital Sodium ◽  
Maze Test

We assessed the effectiveness and mechanism of action of schisandrin on modulation of learning and memory disorders in mice. Memory impairment was established in mice by intraperitoneal injection of pentobarbital sodium (20 mg/kg). Schisandrin (0.5, 1.0, 2.0g/kg) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of schisandrin to reduce phenobarbital-induced learning and memory impairment. The levels of superoxide dismutase (SOD) nitric oxide (NO) and catalase (CAT) were measured in brain tissue samples taken from the mice. Other biomarkers measured included expression of nuclear transcription factor-kappa-B (NF-κB) and brain-derived neurotrophic factor (BDNF) in the hippocampus CA1 region, which were determined by immunohistochemical analysis. On the fifth day of treatment, the mice in the pentobarbital sodium group performed worse on the Morris water maze test compared to untreated controls (P<0.01), which could be prolonged after schisandrin treatment (P<0.05 for="" low="" and="" intermediate="" dose="" groups="" analysis="" of="" brain="" tissues="" showed="" that="" compared="" with="" the="" control="" group="" no="" levels="" were="" increased="" sod="" cat="" activity="" decreased="" in="" pentobarbital="" sodium="" i="">P<0.01). After treatment with schisandrin, the NO levels were significantly decreased (P<0.01), while SOD and CAT activity increased (P<0.01). Immunohistochemistry analysis showed that, in phenobarbital only group, the protein expression of BDNF decreased, NF-κB increased compared to untreated controls, and schisandrin could reverse this trend (P<0.05 and="" i="">P<0.01, respectively). The results suggest that schisandrin is effective in improving the learning and memory deficiency induced by pentobarbital sodium, the mechanism of which may be related modulation of cellular response to oxidative stress.

Microglia, Apoptosis and Interleukin-1β Expression in the Effect of Sophora Japonica L. on Cerebral Infarct Induced by Ischemia-Reperfusion in Rats

2005 ◽  
Vol 33 (03) ◽  
pp. 425-438 ◽  
Author(s):  
Chih-Jui Lao ◽  
Jaung-Geng Lin ◽  
Jon-Son Kuo ◽  
Pei-Dawn Lee Chao ◽  
Chin-Yi Cheng ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Ginkgo Biloba ◽  
Neurological Deficit ◽  
Ischemia Reperfusion ◽  
Cerebral Infarct ◽  
Interleukin 1Β ◽  
Apoptotic Cells ◽  
Sophora Japonica ◽  
Tetrazolium Chloride ◽  
Pre Treatment

Sophora Japonica L. (SJ) is a traditional Chinese herb used to cool blood, stop bleeding and to treat hemorrhoids with bleeding. Although several recent studies found that both SJ and Ginkgo biloba have the same components of quercetin and rutin, only Ginkgo biloba has been widely used to treat cerebrovascular disorders and dementia in humans. This study investigated the effect of SJ on cerebral infarct in rats. A total of 66 Sprague-Dawley (SD) rats were studied. Focal cerebral infarct was established by occluding the bilateral common carotid arteries and the right middle cerebral artery for 90 minutes. After 24 hours of reperfusion, the neurological status was evaluated. The rats were then killed, and brain tissue was stained with 2,3,5-triphenyl-tetrazolium chloride. The grading scale of neurological deficit and the ratio of cerebral infarction area were used as an index to evaluate the effect of SJ on cerebral infarct. In addition, the number of ED1 and interleukin-1β immunostaining positive cells, and apoptotic cells were measured in the cerebral infarction zone. The results indicated that pre-treatment with 100 or 200 mg/kg SJ and post-treatment with 200 mg/kg SJ significantly reduced the grade of neurological deficit and the ratio of cerebral infarction area. In addition, pre-treatment with 200 mg/kg SJ also significantly reduced ED1 and interleukin-1β immunostaining positive cells, and apoptotic cells in ischemia-reperfusion cerebral infarct rats. This study demonstrated that SJ could reduce the cerebral infarction area and neurological deficit induced by ischemia-reperfusion in rats, suggesting its potential as a treatment for cerebral infarct in humans. This effect of SJ involves its suppressive action of microglia, interleukin-1β and apoptosis.

Effects of Panax Notoginseng Saponins on Proliferation and Differentiation of Rat Hippocampal Neural Stem Cells

2011 ◽  
Vol 39 (05) ◽  
pp. 999-1013 ◽  
Author(s):  
Yin-Chu Si ◽  
Jian-Ping Zhang ◽  
Chun-E Xie ◽  
Li-Juan Zhang ◽  
Xiang-Ning Jiang
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Ischemia Reperfusion ◽  
Panax Notoginseng ◽  
Control Group ◽  
Panax Notoginseng Saponins ◽  
Double Labeling ◽  
Proliferation And Differentiation ◽  
Hippocampal Neural Stem Cells

We aimed to investigate the effects of Panax notoginseng saponins (PNS) on proliferation, differentiation and self-renewal of rat hippocampal neural stem cells (NSCs) in vitro. Rat hippocampal NSCs were isolated from post-natal day 1 (P1) rats and cultured in a serum-free medium. The neurospheres were identified by the expressions of nestin, class III β-tublin (Tuj-1) and glial fibrillary acid protein (GFAP). The cells were given PNS and subjected to oxygen glucose deprivation (OGD) as an in vitro model of brain ischemia reperfusion. The proliferation of NSCs was determined by MTT colorimetry, nestin/BrdU immunofluorescent double-labeling and RT-PCR. Differentiation of NSCs was assessed by immunofluorescent double-labeling of nestin/BrdU, nestin/vimentin, and nestin/Tuj-1. The primary cells and the first two passages of cells formed certain amount of neurospheres, the cells derived from a single cell clone also formed neurospheres. Nestin, BrdU, GFAP and Tuj-1-positive cells appeared in those neurospheres. Compared to the control group, PNS significantly promoted NSC proliferation and the expression of nestin/BrdU, and also enhanced Tuj-1, vimentin, and nestin mRNA expressions in hippocampal NSCs. PNS significantly increased area density, optical density and numbers of nestin/BrdU, nestin/vimentin, and nestin/Tuj-1 positive cells following OGD. These results indicate that PNS can promote proliferation and differentiation of hippocampus NCSs in vitro after OGD, suggesting its potential benefits on neurogenesis and neuroregeneration in brain ischemic injury.

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