An examination of neuroprotective effects of 17B-estradiol and extracts from Panax Quinquefolius L., Ginkgo Biloba and Hypericum Perforatum against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced nigral-striatal neuronal degeneration

2001 ◽  
Author(s):  
Wing-yan, Veronica Chan
Keyword(s):  
Ginkgo Biloba ◽  
Hypericum Perforatum ◽  
Neuronal Degeneration ◽  
Panax Quinquefolius ◽  
Neuroprotective Effects

scholarly journals Notoginsenoside R1 attenuates sevoflurane-induced neurotoxicity

2020 ◽  
Vol 11 (1) ◽  
pp. 215-226
Author(s):  
Yibing Zhang ◽  
Yong Zhao ◽  
Yongwang Ran ◽  
Jianyou Guo ◽  
Haifeng Cui ◽  
...  
Keyword(s):  
Neuronal Degeneration ◽  
Apoptotic Cell ◽  
Volatile Anesthetic ◽  
Adenosine Monophosphate ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Sprague Dawley ◽  
Quinone Oxidoreductase ◽  
Neuroprotective Effects ◽  
Cell Counts

AbstractBackgroundSevoflurane, a volatile anesthetic, is known to induce widespread neuronal degeneration and apoptosis. Recently, the stress-inducible protein sestrin 2 and adenosine monophosphate-activated protein kinase (AMPK) have been found to regulate the levels of intracellular reactive oxygen species (ROS) and suppress oxidative stress. Notoginsenoside R1 (NGR1), a saponin isolated from Panax notoginseng, has been shown to exert neuroprotective effects. The effects of NGR1 against neurotoxicity induced by sevoflurane were assessed.MethodsSprague-Dawley rat pups on postnatal day 7 (PD7) were exposed to sevoflurane (3%) anesthesia for 6 h. NGR1 at doses of 12.5, 25, or 50 mg/kg body weight was orally administered to pups from PD2 to PD7.ResultsPretreatment with NGR1 attenuated sevoflurane-induced generation of ROS and reduced apoptotic cell counts. Western blotting revealed decreased cleaved caspase 3 and Bad and Bax pro-apoptotic protein expression. NGR1 substantially upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression along with increased heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase-1 levels, suggesting Nrf2 signaling activation. Enhanced sestrin-2 and phosphorylated AMPK expression were noticed following NGR1 pretreatment.ConclusionThis study revealed the neuroprotective effects of NGR1 through effective suppression of apoptosis and ROS via regulation of apoptotic proteins and activation of Nrf2/HO-1 and sestrin 2/AMPK signaling cascades.

scholarly journals Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Xiao Hu ◽  
Shirong Li ◽  
Desislava Met Doycheva ◽  
Lei Huang ◽  
Cameron Lenahan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Rat Model ◽  
Neuronal Apoptosis ◽  
Neuronal Degeneration ◽  
Infarct Volume ◽  
Neurological Deficits ◽  
Tunel Staining ◽  
Artery Ligation ◽  
Neuroprotective Effects

Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.

562 Caracterization of a model of neuronal degeneration in the gyrus Dentatus of the rat: Neuroprotective effects of anapsos

1996 ◽  
Vol 17 (4) ◽  
pp. S140
Author(s):  
J.J. Miguel-Hidalgo ◽  
L. Fernández-Novoa ◽  
A. Álvarez ◽  
A. Franco ◽  
R. Cacabelos
Keyword(s):  
Neuronal Degeneration ◽  
Neuroprotective Effects ◽  
Gyrus Dentatus

Ginkgo biloba and Its Constituent 6-hydroxykynurenic-acid as well as Its Proanthocyanidins Exert Neurorestorative Effects against Cerebral Ischemia

Planta Medica ◽  
2020 ◽  
Vol 86 (10) ◽  
pp. 696-707
Author(s):  
Jianbiao Yao ◽  
Hongxiang Qiao ◽  
Zhuming Jin ◽  
Ruwei Wang ◽  
Haibo Huang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ginkgo Biloba ◽  
Ischemia Reperfusion ◽  
Grape Seed ◽  
Negative Control ◽  
Major Contributor ◽  
Sprague Dawley ◽  
Neuroprotective Effects ◽  
Phenolic Constituents

AbstractNeuroprotective effects against cerebral ischemia/reperfusion (I/R) injury by Ginkgo biloba leaves are commonly attributed to the antioxidant activity of its proanthocyanidins. Furthermore, preliminary experiments identified 6-hydroxykynurenic acid (6-HKA) as a major contributor to this effect of extract of G. biloba leaves (EGb) prepared according to the Chinese Pharmacopoeia (ChP). In order to elucidate the specific contribution of both proanthocyanidins and 6-HKA to the overall neurorestorative effects of this extract according to ChP, EGb ChP was separated into pure 6-HKA and a newly developed Ginkgo proanthocyanidin extract (GPE), enriched in proanthocyanidins but not containing 6-HKA. Male Sprague-Dawley rats were divided into the groups: sham: 8; model (placebo): 25; GPE 80 mg/kg: 13; GPE 40 mg/kg: 13; GPE 20 mg/kg: 16; grape seed extract (negative control) 40 mg/kg: 18; nimodipine (positive control) 2 mg/kg: 8. All non-sham animals were subjected to cerebral I/R injury by occluding the middle cerebral artery with a nylon suture that was removed after 2 h of ischemia to establish reperfusion. For comparison, a parallel series of experiments were performed with 6-HKA. In these in vivo experiments, neurological dysfunctions were reduced by both GPE and 6-HKA, and both average infarct size and concentrations of malondialdehyde (MDA) and super oxide dismutase (SOD) were significantly ameliorated as compared to the model group. This data, therefore, demonstrates that the neuroprotective effects of EGb cannot be explained by a purely chemical antioxidative effect alone as has been previously proposed, especially with regards to the proanthocyanidins. A pharmacological neurorestorative effect of EGb on neurons and brain tissue itself seems to be a much more straightforward explanation for the presented observations. This effect is most likely explained by the synergistic action of both its numerous phenolic constituents (GPE) and 6-hydroxykynurenic acid (6-HKA), which could be identified as one major contributor to the observed activity.

scholarly journals THE USE OF HERBAL MEDICINE AS COMPLEMENTARY THERAPY FOR THE TREATMENT OF SOME SCHIZOPHRENIA`S SYMPTOMS

2014 ◽  
Vol 15 (3) ◽  
Author(s):  
Fernanda Stumpf TONIN ◽  
Fábio BRASIL ◽  
Ellis Marina SZABO ◽  
Roberto PONTAROLO
Keyword(s):  
Herbal Medicine ◽  
Panax Ginseng ◽  
Ginkgo Biloba ◽  
Hypericum Perforatum ◽  
Complementary Therapy ◽  
Valeriana Officinalis

A esquizofrenia é a mais comum e prevalente psicose, tendo um curso crônico e deteriorativo capaz de impactar na qualidade de vida dos pacientes, familiares e cuidadores. Essa doença afeta as esferas social e ocupacional gerando custos pessoais e financeiros para o paciente e para o sistema de saúde do país. Em termos de tratamento, já existem no mercado diversos fármacos e intervenções disponíveis, sendo usados principalmente antipsicóticos em associação com outras classes de medicamentos (estabilizadores de humor, antidepressivos, benzodiazepínicos). No entanto, além de apresentarem um custo elevado, essas intervenções podem causar diversos sintomas e eventos adversos, o que influencia a adesão e sucesso no tratamento. Nesse contexto, destaca-se o uso de abordagens complementares como as plantas medicinais e a fitoterapia, que tem se mostrado, nas últimas décadas, como uma alternativa viável para auxiliar no tratamento dessa doença. As plantas medicinais são popularmente utilizadas e com isso podem representar um suporte efetivo à terapia medicamentosa de desordens mentais. Este artigo tem como objetivo revisar o uso complementar, bem como a efetividade e segurança de algumas plantas medicinais para o tratamento de sintomas da esquizofrenia. Aparentemente a combinação de plantas medicinais associada à terapia medicamentosa é uma estratégia útil para melhorar a eficácia dos antipsicóticos ou reduzir eventos adversos e custos no tratamento. Foi reportado o uso benéfico de diferentes plantas para o tratamento de sintomas da esquizofrenia incluindo: Erva de São João (Hypericum perforatum) para o tratamento de desordens afetivas e depressão; Valeriana (Valeriana officinalis) para ansiedade e epilepsia; Ginkgo biloba em casos de demência e déficit de memória; Ginseng (Panax ginseng) para pacientes esquizofrênicos com disfunções cognitivas.

scholarly journals Bushen-Yizhi Formula Alleviates Neuroinflammation via Inhibiting NLRP3 Inflammasome Activation in a Mouse Model of Parkinson’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yousheng Mo ◽  
Erjin Xu ◽  
Renrong Wei ◽  
Baoluu Le ◽  
Lei Song ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Neuronal Degeneration ◽  
Interleukin 1 ◽  
Inflammasome Activation ◽  
Neuroprotective Effects ◽  
Nlrp3 Inflammasome Activation

Parkinson’s disease (PD), the second most common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although the molecular mechanisms underlying dopaminergic neuronal degeneration in PD remain unclear, neuroinflammation is considered as the vital mediator in the pathogenesis and progression of PD. Bushen-Yizhi Formula (BSYZ), a traditional Chinese medicine, has been demonstrated to exert antineuroinflammation in our previous studies. However, it remains unclear whether BSYZ is effective for PD. Here, we sought to assess the neuroprotective effects and explore the underlying mechanisms of BSYZ in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine- (MPTP-) induced mouse model of PD. Our results indicate that BSYZ significantly alleviates the motor impairments and dopaminergic neuron degeneration of MPTP-treated mice. Furthermore, BSYZ remarkably attenuates microglia activation, inhibits NLPR3 activation, and decreases the levels of inflammatory cytokines in MPTP-induced mouse brain. Also, BSYZ inhibits NLRP3 activation and interleukin-1βproduction of the 1-methyl-4-phenyl-pyridinium (MPP+) stimulated BV-2 microglia cells. Taken together, our results indicate that BSYZ alleviates MPTP-induced neuroinflammation probably via inhibiting NLRP3 inflammasome activation in microglia. Collectively, BSYZ may be a potential therapeutic agent for PD and the related neurodegeneration diseases.

Neuroprotective effects of Ginkgo biloba extract in brain ischemia are mediated by inhibition of nitric oxide synthesis

Life Sciences ◽  
2000 ◽  
Vol 67 (22) ◽  
pp. 2673-2683 ◽  
Author(s):  
Gioacchino Calapai ◽  
Anna Crupi ◽  
Fabio Firenzuoli ◽  
Maria C. Marciano ◽  
Francesco Squadrito ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Ischemia ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Nitric Oxide Synthesis ◽  
Neuroprotective Effects

scholarly journals Basic FGF, NGF, and IGFs Protect Hippocampal and Cortical Neurons against Iron-Induced Degeneration

1993 ◽  
Vol 13 (3) ◽  
pp. 378-388 ◽  
Author(s):  
Ying Zhang ◽  
Tohru Tatsuno ◽  
John M. Carney ◽  
Mark P. Mattson
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Cortical Neurons ◽  
Hippocampal Neurons ◽  
Neuronal Degeneration ◽  
Cell Damage ◽  
Oxygen Radical ◽  
Neuroprotective Effects ◽  
In Vivo Models

Iron is believed to contribute to the process of cell damage and death resulting from ischemic and traumatic insults by catalyzing the oxidation of protein and lipids. Exposure of cultured rat hippocampal neurons to iron (FeSO4) caused a dose-dependent reduction in neuronal survival, which was potentiated by ascorbate. Damage to neurons was associated with a significant level of oxygen radical in the culture medium. The iron chelator desferal prevented both the neuronal degeneration caused by FeSO4 and the production of oxygen radical, demonstrating that ionic iron was responsible for the cell damage. Iron neurotoxicity was associated with an elevation of [Ca2+]i and was attenuated by NMDA receptor antagonists. Since recent findings demonstrated neuroprotective effects of growth factors in cell culture and in vivo models of ischemia, we examined the effects of growth factors on iron-induced damage. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and insulinlike growth factors (IGF-I and IGF-II) each protected neurons against iron-induced damage. Both rat hippocampal and human cortical neurons were protected by these growth factors. Taken together, the data suggest that the neuroprotective effects of growth factors against excitotoxic/ischemic insults may result, in part, from a prevention or attenuation of oxidative damage.

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