scholarly journals Neuroprotective effect of Scutellaria baicalensis flavones against global ischemic model in rats

2015 ◽  
Vol 27 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Bjakta Prasad Gaire ◽  
Young Ock Kim ◽  
Zhen Hua Jin ◽  
Juyeon Park ◽  
Hoyoung Choi ◽  
...  
Keyword(s):  
Cell Death ◽  
Gastric Ulcer ◽  
Methanol Extract ◽  
Biological Effects ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Alternative Therapies ◽  
Scutellaria Baicalensis ◽  
Scutellaria Baicalensis Georgi

Scutellaria baicalensis Georgi (SB) is the medicinal plants mainly used in traditional Chinese medicine. It has been used for the treatment of various chronic inflammatory syndromes including respiratory disease, fever and gastric ulcer in traditional Eastern medicine and its major components; baicalin, baicalein and wogonin; were reported to have various biological effects. The aim of this study was to isolate the neuroprotective flavones from the root of S. baicalensis (SB) by bioactivity-guided fractionation of S. baicalensis methanol extract (SBME). Neuroprotective effect of isolated flavones, namely was studied on global ischemic model in rat by 4-VO. SBME was fractionated with different solvent and resulting fractions were administered at a dose of 25 mg/kg to the rat and potent neuroprotective fractions were sub-fractionated. At a dose of 10 mg/kg, isolated compounds, wogonin, and baicalein inhibited the hippocampal neuronal cell death by 78.6% and 81.0% respectively. Our study suggested that SB and its isolated flavones have potential neuroprotective effect and these findings may be one of the alternative therapies for the management of stroke and other neurodegenerative diseases. DOI: http://dx.doi.org/10.3126/jnpa.v27i1.12144 Journal of Nepal Pharmaceutical Association 2014 Vol.XXVII: 1-8

scholarly journals NMDA Receptor-Mediated Neuroprotective Effect of theScutellaria baicalensisGeorgi Extract on the Excitotoxic Neuronal Cell Death in Primary Rat Cortical Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Cell Cultures ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Cortical Cell ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Phytochemical Analysis ◽  
Cortical Cell Cultures

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.

scholarly journals Protective Effects of Active Compounds from Salviae miltiorrhizae Radix against Glutamate-Induced HT-22 Hippocampal Neuronal Cell Death

Processes ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 914
Author(s):  
Hung Manh Phung ◽  
Sullim Lee ◽  
Ki Sung Kang
Keyword(s):  
Cell Death ◽  
Rosmarinic Acid ◽  
Calcium Influx ◽  
Salvia Miltiorrhiza ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Salvianolic Acid B ◽  
Tanshinone Iia ◽  
Salvianolic Acid

Oxidative stress is considered one of the factors that cause dysfunction and damage of neurons, causing diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD).Recently, natural antioxidant sources have emerged as one of the main research areas for the discovery of potential neuroprotectants that can be used to treat neurological diseases. In this research, we assessed the neuroprotective effect of a 70% ethanol Salvia miltiorrhiza Radix (SMR) extract and five of its constituent compounds (tanshinone IIA, caffeic acid, salvianolic acid B, rosmarinic acid, and salvianic acid A) in HT-22 hippocampal cells. The experimental data showed that most samples were effective in attenuating the cytotoxicity caused by glutamate in HT-22 cells, except for rosmarinic acid and salvianolic acid B. Of the compounds tested, tanshinone IIA (TS-IIA) exerted the strongest effect in protecting HT-22 cells against glutamate neurotoxin. Treatment with 400 nM TS-IIA restored HT-22 cell viability almost completely. TS-IIA prevented glutamate-induced oxytosis by abating the accumulation of calcium influx, reactive oxygen species, and phosphorylation of mitogen-activated protein kinases. Moreover, TS-IIA inhibited glutamate-induced cytotoxicity by reducing the activation and phosphorylation of p53, as well as by stimulating Akt expression. This research suggested that TS-IIA is a potential neuroprotective component of SMR, with the ability to protect against neuronal cell death induced by excessive amounts of glutamate.

scholarly journals Ghrelin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

2010 ◽  
Vol 205 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Jiyeon Lee ◽  
Eunjin Lim ◽  
Yumi Kim ◽  
Endan Li ◽  
Seungjoon Park
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Therapeutic Potential ◽  
Excitatory Amino Acid ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Proinflammatory Mediators ◽  
Hippocampal Neurodegeneration

Ghrelin is an endogenous ligand for GH secretagogue receptor type 1a (GHSR1a), and is produced and released mainly from the stomach. It has been recently demonstrated that ghrelin can function as a neuroprotective factor by inhibiting apoptotic pathways. Kainic acid (KA), an excitatory amino acid l-glutamate analog, causes neuronal death in the hippocampus; previous studies suggest that activated microglia and astrocytes actively participate in the pathogenesis of KA-induced hippocampal neurodegeneration. However, it is unclear whether ghrelin has neuroprotective effect in KA-induced hippocampal neurodegeneration. I.p. injection of KA produced typical neuronal cell death in the CA1 and CA3 pyramidal layers of the hippocampus, and the systemic administration of ghrelin significantly attenuated KA-induced neuronal cell death in these regions through the activation of GHSR1a. Ghrelin prevents KA-induced activation of microglia and astrocytes, and the expression of proinflammatory mediators tumor necrosis factor α, interleukin-1β, and cyclooxygenase-2. The inhibitory effect of ghrelin on the activation of microglia and astrocytes appears to be associated with the inhibition of matrix metalloproteinase-3 expression in damaged hippocampal neurons. Our data suggest that ghrelin has a therapeutic potential for suppressing KA-induced pathogenesis in the brain.

scholarly journals Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-30 ◽  
Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen
Keyword(s):  
Cell Death ◽  
Natural Products ◽  
Neurodegenerative Diseases ◽  
Bioactive Compounds ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuronal Structure ◽  
And Function

In recent years, natural products, which originate from plants, animals, and fungi, together with their bioactive compounds have been intensively explored and studied for their therapeutic potentials for various diseases such as cardiovascular, diabetes, hypertension, reproductive, cancer, and neurodegenerative diseases. Neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are characterized by the progressive dysfunction and loss of neuronal structure and function that resulted in the neuronal cell death. Since the multifactorial pathological mechanisms are associated with neurodegeneration, targeting multiple mechanisms of actions and neuroprotection approach, which involves preventing cell death and restoring the function to damaged neurons, could be promising strategies for the prevention and therapeutic of neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for the treatment of neurodegenerative diseases. This review focused on the therapeutic potential of natural products and their bioactive compounds to exert a neuroprotective effect on the pathologies of neurodegenerative diseases.

scholarly journals Hypothermia Reduces Toll-Like Receptor 3-Activated Microglial Interferon-βand Nitric Oxide Production

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Tomohiro Matsui ◽  
Yukari Motoki ◽  
Yusuke Yoshida
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Therapeutic Hypothermia ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Dependent Manner ◽  
Cns Injury ◽  
Concentration Dependent Manner ◽  
Polycytidylic Acid

Therapeutic hypothermia protects neurons after injury to the central nervous system (CNS). Microglia express toll-like receptors (TLRs) that play significant roles in the pathogenesis of sterile CNS injury. To elucidate the possible mechanisms involved in the neuroprotective effect of therapeutic hypothermia, we examined the effects of hypothermic culture on TLR3-activated microglial release of interferon (IFN)-βand nitric oxide (NO), which are known to be associated with neuronal cell death. When rat or mouse microglia were cultured under conditions of hypothermia (33°C) and normothermia (37°C) with a TLR3 agonist, polyinosinic-polycytidylic acid, the production of IFN-βand NO in TLR3-activated microglia at 48 h was decreased by hypothermia compared with that by normothermia. In addition, exposure to recombinant IFN-βand sodium nitroprusside, an NO donor, caused death of rat neuronal pheochromocytoma PC12 cells in a concentration-dependent manner after 24 h. Taken together, these results suggest that the attenuation of microglial production of IFN-βand NO by therapeutic hypothermia leads to the inhibition of neuronal cell death.

scholarly journals Neuroprotective γ-Pyrones from Fusarium Solani JS-0169: Cell-Based Identification of Active Compounds and an Informatics Approach to Predict the Mechanism of Action

Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 91 ◽  
Author(s):  
Hyun Gyu Choi ◽  
Ji Hoon Song ◽  
Musun Park ◽  
Soonok Kim ◽  
Chang-Eop Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Fusarium Solani ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuroprotective Activity ◽  
Glutamate Toxicity ◽  
Protective Effects ◽  
Cns Injury ◽  
Ht22 Cells

Glutamate toxicity has been implicated in neuronal cell death in both acute CNS injury and in chronic diseases. In our search for neuroprotective agents obtained from natural sources that inhibit glutamate toxicity, an endophytic fungus, Fusarium solani JS-0169 isolated from the leaves of Morus alba, was found to show potent inhibitory activity. Chemical investigation of the cultures of the fungus JS-0169 afforded isolation of six compounds, including one new γ-pyrone (1), a known γ-pyrone, fusarester D (2), and four known naphthoquinones: karuquinone B (3), javanicin (4), solaniol (5), and fusarubin (6). To identify the protective effects of the isolated compounds (1–6), we assessed their inhibitory effect against glutamate-induced cytotoxicity in HT22 cells. Among the isolates, compound 6 showed significant neuroprotective activity on glutamate-mediated HT22 cell death. In addition, the informatics approach using in silico systems pharmacology identified that compound 6 may exert its neuroprotective effect by controlling the amount of ubiquinone. The results suggest that the metabolites produced by the endophyte Fusarium solani JS-0169 might be related to the neuroprotective activity of its host plant, M. alba.

Neuroprotective effect of 1-methoxyoctadecan-1-ol from Uncaria sinensis on glutamate-induced hippocampal neuronal cell death

2014 ◽  
Vol 155 (1) ◽  
pp. 293-299 ◽  
Author(s):  
Sung Min Ahn ◽  
Ha Neui Kim ◽  
Yu Ri Kim ◽  
Eun Young Oh ◽  
Young Whan Choi ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Carbon Monoxide Modulation of Microglia-neuron Communication: Anti-neuroinflammatory and Neurotrophic Role

2021 ◽  
Author(s):  
Nuno L. Soares ◽  
Inês Paiva ◽  
Joana Bravo ◽  
Claudia S. F. Queiroga ◽  
Bernadete F. Melo ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cell Death ◽  
Neuroprotective Effect ◽  
Primary Cultures ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuronal Morphology ◽  
Conditioned Media ◽  
Inflammatory Factors ◽  
Remote Communication

Abstract Microglia, the ‘resident immunocompetent cells’ of the central nervous system (CNS), are key players in innate immunity, synaptic refinement and homeostasis. Dysfunctional microglia contribute heavily to creating a toxic inflammatory milieu, a driving factor in the pathophysiology of several CNS disorders. Therefore, strategies to modulate the microglial function are required to tackle exacerbated tissue inflammation. Carbon monoxide (CO), an endogenous gaseous molecule produced by the degradation of haem, has anti-inflammatory, anti-apoptotic, pro-homeostatic and cytoprotective roles, among others.ALF826A, a novel molybdenum-based CO-releasing molecule, was used for the assessment of neuron-microglia remote communication. Primary cultures of rat microglia and neurons, or the BV-2 microglial and CAD neuronal murine cell lines, were used to study the microglia-neuron interaction. An approach based on microglial-derived conditioned media in neuronal culture was applied. Medium derived from CO-treated microglia provided indirect neuroprotection against inflammation by limiting the lipopolysaccharide (LPS)-induced expression of reactivity markers (CD11b), the production of reactive oxygen species (ROS) and the secretion of inflammatory factors (TNF-α, nitrites). This consequently prevented neuronal cell death and maintained neuronal morphology In contrast, in the absence of inflammatory stimulus, conditioned media from CO-treated microglia improved neuronal morphological complexity, which is an indirect manner of assessing neuronal function. Likewise, the microglial medium also prevented neuronal cell death induced by pro-oxidant tert-Butyl hydroperoxide (t-BHP). ALF826 treatment reinforced microglia secretion of Interleukin-10 (IL-10) and adenosine, mediators that may protect against t-BHP stress in this remote communication model. Chemical inhibition of the adenosine receptors A2A and A1 reverted the CO-derived neuroprotective effect, further highlighting a role for CO in regulating neuron-microglia communication via purinergic signalling.Our findings indicate that CO has a modulatory role on microglia-to-neuron communication, promoting neuroprotection in a non-cell autonomous manner. CO enhances the microglial release of neurotrophic factors and blocks exacerbated microglial inflammation. CO improvement of microglial neurotrophism under non-inflammatory conditions is here described for the first time.

scholarly journals Resveratrol modulates the Akt/GSK-3β signaling pathway in a middle cerebral artery occlusion animal model

2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Dong-Ju Park ◽  
Ju-Bin Kang ◽  
Fawad-Ali Shah ◽  
Phil-Ok Koh
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Signaling Pathway ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Gsk 3Β ◽  
Cerebral Artery Occlusion

Abstract Cerebral ischemia is a major cause of neurodegenerative disease. It induces neuronal vulnerability and susceptibility, and leads to neuronal cell death. Resveratrol is a polyphenolic compound that acts as an anti-oxidant. It exerts a neuroprotective effect against focal cerebral ischemic injury. Akt signaling pathway is accepted as a representative cell survival pathway, including proliferation, growth, and glycogen synthesis. This study investigated whether resveratrol regulates Akt/glycogen synthase kinase-3β (GSK-3β) pathway in a middle cerebral artery occlusion (MCAO)-induced ischemic brain injury. Adult male rats were intraperitoneally injected with vehicle or resveratrol (30 mg/kg) and cerebral cortices were isolated 24 h after MCAO. Neurological behavior test, corner test, brain edema measurment, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of resveratrol. Phospho-Akt and phospho-GSK-3β expression levels were measured using Western blot analysis. MCAO injury led to severe neurobehavioral deficit, infraction, and histopathological changes in cerebral cortex. However, resveratrol treatment alleviated these changes caused by MCAO injury. Moreover, MCAO injury induced decreases in phospho-Akt and phospho-GSK-3β protein levels, whereas resveratrol attenuated these decreases. Phosphorylations of Akt and GSK-3β act as a critical role for the suppression of apoptotic cell death. Thus, our finding suggests that resveratrol attenuates neuronal cell death in MCAO-induced cerebral ischemia and Akt/GSK-3β signaling pathway contributes to the neuroprotective effect of resveratrol.

scholarly journals Synergistic Neuroprotective Effect of Schisandra chinensis and Ribes fasciculatum on Neuronal Cell Death and Scopolamine-Induced Cognitive Impairment in Rats

2019 ◽  
Vol 20 (18) ◽  
pp. 4517
Author(s):  
Eunkuk Park ◽  
Min Jeong Ryu ◽  
Nam Ki Kim ◽  
Mun Hyoung Bae ◽  
Youngha Seo ◽  
...  
Keyword(s):  
Cell Death ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Passive Avoidance ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Schisandra Chinensis ◽  
Maze Test

Mild cognitive impairment (MCI) is considered as a transitional stage between aging and Alzheimer’s disease. In the present study, we examined the protective effect of Schisandra chinensis (SC) and Ribes fasciculatum (RF) on neuronal cell death in vitro and scopolamine-induced cognitive impairment in Sprague Dawley® rats in vivo. A mixture of SC and RF extracts (SC+RF) significantly protected against hydrogen peroxide-induced PC12 neuronal cell death. The neuroprotective effect of SC+RF on scopolamine-induced memory impairment in rats was evaluated using the passive avoidance test and the Morris water maze test. In the passive avoidance test, SC+RF-treated rats showed an increased latency to escape, compared to the scopolamine-treated rats. Moreover, SC+RF treatment significantly reduced escape latency in water maze test, compared to treatment with scopolamine alone. To verify the long-term memory, we performed probe test of water maze test. As a result, rat treated with SC+RF spent more time in the target quadrant. Consistent with enhancement of memory function, the brain derived neurotrophic factor (BDNF) and its downstream molecules (pERK, pATK, and pCREB) are increased in SC+RF treatment in hippocampal area compared with scopolamine treated group. These results suggest that a mixture of SC and RF extracts may be a good therapeutic candidate for preventing mild cognitive impairment.

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