scholarly journals Chrysin Protects against Memory and Hippocampal Neurogenesis Depletion in D-Galactose-Induced Aging in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1100
Author(s):  
Ram Prajit ◽  
Nataya Sritawan ◽  
Kornrawee Suwannakot ◽  
Salinee Naewla ◽  
Anusara Aranarochana ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Survival ◽  
Brain Aging ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Hippocampal Neurogenesis ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Novel Object ◽  
Immature Neurons

The interruption of hippocampal neurogenesis due to aging impairs memory. The accumulation of D-galactose (D-gal), a monosaccharide, induces brain aging by causing oxidative stress and inflammation, resulting in neuronal cell damage and memory loss. Chrysin, an extracted flavonoid, has neuroprotective effects on memory. The present study aimed to investigate the effect of chrysin on memory and hippocampal neurogenesis in brains aged using D-gal. Male Sprague-Dawley rats received either D-gal (50 mg/kg) by i.p. injection, chrysin (10 or 30 mg/kg) by oral gavage, or D-gal (50 mg/kg) and chrysin (10 or 30 mg/kg) for 8 weeks. Memory was evaluated using novel object location (NOL) and novel object recognition (NOR) tests. Hippocampal neurogenesis was evaluated using Ki-67, 5-bromo-2′-deoxyuridine (BrdU), and doublecortin (DCX) immunofluorescence staining to determine cell proliferation, cell survival, and number of immature neurons, respectively. We found that D-gal administration resulted in memory impairment as measured by NOL and NOR tests and in depletions in cell proliferation, cell survival, and immature neurons. However, co-treatment with chrysin (10 or 30 mg/kg) attenuated these impairments. These results suggest that chrysin could potentially minimize memory and hippocampal neurogenesis depletions brought on by aging.

scholarly journals Hesperidin Alleviates Methotrexate-Induced Memory Deficits via Hippocampal Neurogenesis in Adult Rats

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 936 ◽  
Author(s):  
Salinee Naewla ◽  
Apiwat Sirichoat ◽  
Wanassanan Pannangrong ◽  
Pornthip Chaisawang ◽  
Peter Wigmore ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Memory Loss ◽  
Memory Deficits ◽  
Hippocampal Neurogenesis ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Ki 67 ◽  
Novel Object ◽  
Immature Neurons

Methotrexate (MTX), a folic acid antagonist, is widely used in cancer treatment. However, treatment with MTX reduces hippocampal neurogenesis, leading to memory deficits. Hesperidin (Hsd) is a flavonoid glycoside that promotes anti-inflammation, acts as an antioxidant, and has neuroprotective properties. Consumption of Hsd enhances learning and memory. In the present study, we investigated the protective effects of Hsd against MTX-induced impairments of memory and neurogenesis; male Sprague Dawley rats were administered with a single dose of MTX (75 mg/kg) by intravenous (i.v.) injection on days 8 and 15 or Hsd (100 mg/kg) by oral gavage for 21 days. Memory was tested using novel object location (NOL) and novel object recognition (NOR) tasks. Immunofluorescence staining of Ki-67, bromodeoxyuridine (BrdU), and doublecortin (DCX) was performed to assess cell proliferation, survival, and immature neurons. The data showed that Hsd and MTX did not disable locomotor ability. The MTX animals exhibited memory deficits in both memory tests. There were significant decreases in the numbers of cell proliferation, survival, and immature neurons in the MTX animals. However, co-administration with MTX and Hsd alleviated memory loss and neurogenesis decline. These results revealed that Hsd could protect against MTX side effects in the animals in this study.

scholarly journals AC-YVAD-CMK Inhibits Pyroptosis and Improves Functional Outcome after Intracerebral Hemorrhage

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao Lin ◽  
Haotuo Ye ◽  
Felix Siaw-Debrah ◽  
Sishi Pan ◽  
Zibin He ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracerebral Hemorrhage ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Neurological Function ◽  
Inflammatory Factors ◽  
Neuroprotective Effects ◽  
Caspase 1 ◽  
Cell Death Pathways ◽  
Cell Death Pathway

Intracerebral hemorrhage (ICH) refers to bleeding in the brain and is associated with the release of large amount of inflammasomes, and the activation of different cell death pathways. These cell death pathways lead to removal of inactivated and damaged cells and also result in neuronal cell damage. Pyroptosis is a newly discovered cell death pathway that has gained attention in recent years. This pathway mainly depends on activation of caspase-1-mediated cascades to cause cell death. We tested a well-known selective inhibitor of caspase-1, AC-YVAD-CMK, which has previously been found to have neuroprotective effects in ICH mice model, to ascertain its effects on the activation of inflammasomes mediated pyroptosis. Our results showed that AC-YVAD-CMK could reduce caspase-1 activation and inhibit IL-1β production and maturation, but has no effect on NLRP3 expression, an upstream inflammatory complex. AC-YVAD-CMK administration also resulted in reduction in M1-type microglia polarization around the hematoma, while increasing the number of M2-type cells. Furthermore, AC-YVAD-CMK treated mice showed some recovery of neurological function after hemorrhage especially at the hyperacute and subacute stage resulting in some degree of limb movement. In conclusion, we are of the view that AC-YVAD-CMK could inhibit pyroptosis, decrease the secretion or activation of inflammatory factors, and affect the polarization of microglia resulting in improvement of neurological function after ICH.

Rosmarinic acid mediated neuroprotective effects against H2O2-induced neuronal cell damage in N2A cells

Life Sciences ◽  
2014 ◽  
Vol 113 (1-2) ◽  
pp. 7-13 ◽  
Author(s):  
Hadi Ghaffari ◽  
M. Venkataramana ◽  
Behrouz Jalali Ghassam ◽  
S. Chandra Nayaka ◽  
A. Nataraju ◽  
...  
Keyword(s):  
Rosmarinic Acid ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
N2a Cells

scholarly journals Molecular Targets Involved in the Neuroprotection Mediated by Terpenoids

Planta Medica ◽  
2019 ◽  
Vol 85 (17) ◽  
pp. 1304-1315 ◽  
Author(s):  
Laura González-Cofrade ◽  
Beatriz de las Heras ◽  
Luis Apaza Ticona ◽  
Olga M. Palomino
Keyword(s):  
Therapeutic Potential ◽  
Cell Damage ◽  
Biological Activities ◽  
Neuronal Cell ◽  
Molecular Targets ◽  
Research Activity ◽  
Neuroprotective Effects ◽  
Therapeutic Value ◽  
Wide Range ◽  
Drug Leads

AbstractNatural products and their derivatives represent the most consistently successful source of drug leads. Terpenoids, a structurally diverse group, are secondary metabolites widely distributed in nature, endowed with a wide range of biological activities such as antibacterial, anti-inflammatory, antitumoral, or neuroprotective effects, which consolidate their therapeutic value. During the last decades, and taking into consideration the prevalence of aging-related diseases, research activity into the neuroprotective effects of these types of compounds has increased enormously. Several signaling pathways involved in neuroprotection are targets of their mechanism of action and mediate their pleiotropic protective activity in neuronal cell damage. In the present review, molecular basis of the neuroprotection exerted by terpenoids is presented, focusing on preclinical evidence of the therapeutic potential of diterpenoids and triterpenoids on neurodegenerative disorders. By acting on diverse mechanisms simultaneously, terpenoids have been emphasized as promising multitarget agents.

scholarly journals Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

2021 ◽  
Author(s):  
Yasaman Razavi ◽  
Fariborz Keyhanfar ◽  
Abbas Haghparast ◽  
Ronak Shabani ◽  
Mehdi Mehdizadeh
Keyword(s):  
Dentate Gyrus ◽  
Chronic Exposure ◽  
Neuronal Degeneration ◽  
Hippocampal Neurogenesis ◽  
Control Group ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Promising Therapeutic Approach ◽  
Abstinence Period

Abstract Chronic methamphetamine (meth) abuse can lead to certain deficits in the hippocampal function by affecting the hippocampal neurogenesis and plasticity. To determine whether cannabidiol (CBD) can promote proliferation and maturation of neuronal progenitor cells, this study investigated the CBD effect on neurogenesis in the hippocampal dentate gyrus (DG) following chronic exposure to meth in rats. The rats received 2 mg/kg of meth twice a day for ten days. Next, immunofluorescence was performed to evaluate the effect of intracerebroventricular (ICV) administration of CBD (50 µg/5 µL) over an abstinence period (ten days) on the expression levels of neurogenesis markers, such as Ki67, NeuN, and doublecortin (DCX). Moreover, neuronal degeneration in the hippocampus was assessed using Nissl staining. According to our findings, repeated ICV administration of CBD improved cell proliferation and neurogenesis and increased the number of Ki-67 and DCX-positive cells in the abstinence period. Meanwhile, meth treatment subjects caused a significant decrease in the number of neurogenesis makers, as compared to the control group. The neurogenesis markers (Ki-67 and DCX) could be somewhat reversed, while NeuN did not show any significant increase in the CBD group. Our findings demonstrated that CBD can induce neuroprotective effects by modulating neurogenesis. Therefore, it can provide a promising therapeutic approach to improve cognitive performance following chronic exposure to psychostimulant drugs, including meth.

scholarly journals Contribution of ginsenosides Rg1, Rb1 to the neuroprotective effect of Panax notoginseng in mouse organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation

2021 ◽  
Vol 63 (2) ◽  
pp. 64-69
Author(s):  
Nguyen Thi Thanh Loan ◽  
◽  
Le Thi Xoan ◽  
Pham Thi Nguyet Hang ◽  
Nguyen Van Tai ◽  
...  
Keyword(s):  
Hippocampal Slice ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Panax Notoginseng ◽  
Ginsenoside Rg1 ◽  
Neuroprotective Effects ◽  
Oxygen And Glucose Deprivation ◽  
Mk 801

We previously demonstrated that Panax notoginseng (pNG) root extract treatments exertedneuroprotective effects on brain injuries using middle cerebral artery occlusion in mice. The present study aims to investigate the neuroprotective effects of PNG extract and its ginsenosides Rg1 and Rb1 on ischemic neuronal damage caused by oxygen and glucose deprivation (OGD) in mouse organotypic hippocampal slice cultures (OHSCs). Before the experiments, hippocampal slices collected from 7-day-old Swiss mice were cultured for 7 days. OGD was triggered in OHSCs for 30, 60, or 90 min with the aim of finding the optimal period of OGD for drug testing. PNG extract (10, 30 μg/ml), ginsenosides Rg1 and Rb1 (5, 25 μM), or MK-801 25 μM, a reference drug, was added to the culture medium 24 h before OGD and these treatments were continued for 24 h after the optimum 60-min period of OGD. After 24 h of OGD exposure, the measurement of propidium iodide uptake was analysed in OHSCs to evaluate neuronal cell damage. The results showed that OGD time-dependently increased PI uptake of the OHSCs. PNG 30 μg/ml treatment reduced the OGD-induced neuronal cell damage in OHSCs. Ginsenosides Rg1 25 μM, Rb1 (5, 25 μM), as well as MK-801 (25 μM) significantly inhibited PI uptake 24 h after OGD exposure. However, ginsenoside Rg1 5 μM did not show any significant effects on the OGD-induced neuronal cell damage. These findings indicated that ginsenosides Rg1 and Rb1 contributed to the neuroprotective effects of PNG against ischemic damage in OHSCs and the neuroprotective effect of ginsenoside Rb1 was stronger than that of ginsenoside Rg1.

scholarly journals Minocycline Increases in-vitro Cortical Neuronal Cell Survival after Laser Induced Axotomy

2020 ◽  
Vol 15 (2) ◽  
pp. 105-109 ◽  
Author(s):  
Burak Yulug ◽  
Mehmet Ozansoy ◽  
Merve Alokten ◽  
Muzaffer B.C. Ozansoy ◽  
Seyda Cankaya ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
Therapeutic Trials ◽  
Trauma Model ◽  
Injury Models ◽  
Translational Block

Background: Antibiotic therapies targeting multiple regenerative mechanisms have the potential for neuroprotective effects, but the diversity of experimental strategies and analyses of non-standardised therapeutic trials are challenging. In this respect, there are no cases of successful clinical application of such candidate molecules when it comes to human patients. Methods: After 24 hours of culturing, three different minocycline (Sigma-Aldrich, M9511, Germany) concentrations (1 μM, 10 μM and 100 μM) were added to the primary cortical neurons 15 minutes before laser axotomy procedure in order to observe protective effect of minocycline in these dosages. Results: Here, we have shown that minocycline exerted a significant neuroprotective effect at 1 and 100μM doses. Beyond confirming the neuroprotective effect of minocycline in a more standardised and advanced in-vitro trauma model, our findings could have important implications for future studies that concentrate on the translational block between animal and human studies. Conclusion: Such sophisticated approaches might also help to conquer the influence of humanmade variabilities in critical experimental injury models. To the best of our knowledge, this is the first study showing that minocycline increases in-vitro neuronal cell survival after laser-axotomy.

scholarly journals In Vivo Induction of Glial Cell Proliferation and Axonal Outgrowth and Myelination by Brain-Derived Neurotrophic Factor

2006 ◽  
Vol 20 (11) ◽  
pp. 2987-2998 ◽  
Author(s):  
Dorien M. de Groot ◽  
Anton J. M. Coenen ◽  
Albert Verhofstad ◽  
François van Herp ◽  
Gerard J. M. Martens
Keyword(s):  
Cell Proliferation ◽  
Cell Survival ◽  
Glial Cell ◽  
Glial Cells ◽  
Neurotrophic Factor ◽  
Transgene Expression ◽  
Neuronal Cell ◽  
Axonal Outgrowth ◽  
Glial Cell Proliferation

Abstract Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of neuronal cell survival and differentiation factors but is thought to be involved in neuronal cell proliferation and myelination as well. To explore the role of BDNF in vivo, we employed the intermediate pituitary melanotrope cells of the amphibian Xenopus laevis as a model system. These cells mediate background adaptation of the animal by producing high levels of the prohormone proopiomelanocortin (POMC) when the animal is black adapted. We used stable X. transgenesis in combination with the POMC gene promoter to generate transgenic frogs overexpressing BDNF specifically and physiologically inducible in the melanotrope cells. Intriguingly, an approximately 25-fold overexpression of BDNF resulted in hyperplastic glial cells and myelinated axons infiltrating the pituitary, whereby the transgenic melanotrope cells became located dispersed among the induced tissue. The infiltrating glial cells and axons originated from both peripheral and central nervous system sources. The formation of the phenotype started around tadpole stage 50 and was induced by placing white-adapted transgenics on a black background, i.e. after activation of transgene expression. The severity of the phenotype depended on the level of transgene expression, because the intermediate pituitaries from transgenic animals raised on a white background or from transgenics with only an approximately 5-fold BDNF overexpression were essentially not affected. In conclusion, we show in a physiological context that, besides its classical role as neuronal cell survival and differentiation factor, in vivo BDNF can also induce glial cell proliferation as well as axonal outgrowth and myelination.

scholarly journals Protective Effects of p-Coumaric Acid Isolated from Vaccinium bracteatum Thunb. Leaf Extract on Corticosterone-Induced Neurotoxicity in SH-SY5Y Cells and Primary Rat Cortical Neurons

Processes ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 869
Author(s):  
Dool-Ri Oh ◽  
Moon-Jong Kim ◽  
Eun-Jin Choi ◽  
Yujin Kim ◽  
Hak-Sung Lee ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Cell Damage ◽  
Primary Cultures ◽  
Water Extract ◽  
Neuronal Cell ◽  
Protective Effects ◽  
Coumaric Acid ◽  
Cortical Cells ◽  
Neuroprotective Effects ◽  
Creb Phosphorylation

Corticosterone (CORT)-induced oxidative stress and neurotoxicity can cause neuronal dysfunction and mental disorders. In the present study, we investigated the effects and mechanism of the HP-20 resin fraction of the water extract of Vaccinium bracteatum leaves (NET-D1602) and its bioactive compound p-coumaric acid on neuronal cell damage in SH-SY5Y cells and primary culture of rat cortical cells. NET-D1602 and p-coumaric acid significantly improved cell viability in CORT-induced neurotoxicity in SH-SY5Y cells and primary cultures of rat cortical cells, and increased the activities of antioxidant enzymes (superoxide dismutase and catalase) against CORT-induced neurotoxicity in SH-SY5Y cells. NET-D1602 and p-coumaric acid increased the phosphorylation levels of ERK1/2 and cAMP response element-binding protein (CREB) in cortical neurons. In addition, CREB phosphorylation by NET-D1602 and p-coumaric acid was dramatically reversed by PKA, c-Raf/ERK, PI3K, and mTOR inhibitors. Lastly, we demonstrated the neuroprotective effects of NET-D1602 (3 and 10 μg/mL) and p-coumaric acid (3 and 10 μM) via increased CREB phosphorylation in CORT-induced neurotoxicity mediated via the ERK1/2, Akt, and mTOR pathways. These results suggest that p-coumaric acid is a potential neuroprotective component of NET-D1602, with the ability to protect against CORT-induced neurotoxicity by regulating ERK1/2, Akt, and mTOR-mediated CREB phosphorylation.

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.

Sign in / Sign up

Export Citation Format

Share Document