19 results on '"Amin, Faiz Ul"'
Search Results
2. Natural Dietary Supplementation of Anthocyanins via PI3K/Akt/Nrf2/HO-1 Pathways Mitigate Oxidative Stress, Neurodegeneration, and Memory Impairment in a Mouse Model of Alzheimer’s Disease
- Author
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Ali, Tahir, Kim, Taehyun, Rehman, Shafiq Ur, Khan, Muhammad Sohail, Amin, Faiz Ul, Khan, Mehtab, Ikram, Muhammad, and Kim, Myeong Ok
- Published
- 2018
- Full Text
- View/download PDF
3. Glycine inhibits ethanol-induced oxidative stress, neuroinflammation and apoptotic neurodegeneration in postnatal rat brain
- Author
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Amin, Faiz Ul, Shah, Shahid Ali, and Kim, Myeong Ok
- Published
- 2016
- Full Text
- View/download PDF
4. Protective Effect of Lupeol Against Lipopolysaccharide-Induced Neuroinflammation via the p38/c-Jun N-Terminal Kinase Pathway in the Adult Mouse Brain
- Author
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Badshah, Haroon, Ali, Tahir, Rehman, Shafiq-ur, Amin, Faiz-ul, Ullah, Faheem, Kim, Tae Hyun, and Kim, Myeong Ok
- Published
- 2016
- Full Text
- View/download PDF
5. Melatonin Stimulates the SIRT1/Nrf2 Signaling Pathway Counteracting Lipopolysaccharide (LPS)‐Induced Oxidative Stress to Rescue Postnatal Rat Brain
- Author
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Shah, Shahid Ali, Khan, Mehtab, Jo, Myeung‐Hoon, Jo, Min Gi, Amin, Faiz Ul, and Kim, Myeong Ok
- Published
- 2017
- Full Text
- View/download PDF
6. Synthesis of Silver Nanoparticles from Anagalis arvensis and Their Biomedical Applications
- Author
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Shah, Mohib, Anwar, Natasha, Saleem, Samreen, Munir, Iqbal, Shah, Niaz Ali, Fida, Baseerat, Khan, Abbas, Hussain, Anwar, and Amin, Faiz Ul
- Subjects
biology_other - Abstract
Background. Nanotechnology is promising field for generating new applications. A green synthesis of nanoparticles through biological methods using plant extract have a reliable and ecofriendly approach to improve our global environment. Methods. Silver nanoparticles (AgNPs) were synthesized using aqueous extract of Anagalis arvensis L and silver nitrate and were physicochemically characterized. Results. The stability of AgNPs toward acidity, alkalinity, salinity and temperature showed that they remained stable at room temperature for more than two months. The SEM and TEM analysis of the AgNPs showed that they have a uniform spherical shape with an average size in the range of 40–78 nm. Further 1-Dibhenyl-2-Picrylhydrazl radical in Anagalis arvensis L.mediated AgNPs showed a maximum activity of 98% at concentration of 200μg/mL. Hydrogen peroxide scavenging assay in Anagalis arvensis L. mediated AgNPs showed a maximum activity of 85% at concentration of 200μg/mL. Reducing power of Anagalis arvensis L.Ag NPs exhibited a higher activity of 330 μg/mL at concentration of 200 μg/mL. These NPs have cytotoxic effects against brine shrimp (Artemia salina) nauplii with a value of 53% LD 178.04μg/mL. Conclusion. The AgNPs synthesized usingAnagalis arvensis L. extract demonstrate a broad range of applications.
- Published
- 2018
7. Synergistic effect of silver nanoparticles and polymyxin B against biofilm produced by Pseudomonas aeruginosa isolates of pus samples in vitro.
- Author
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Salman, Muhammad, Rizwana, Rizwana, Khan, Hayat, Munir, Iqbal, Hamayun, Muhammad, Iqbal, Aquib, Rehman, Abdul, Amin, Khalid, Ahmed, Ghayour, Khan, Majid, Khan, Ajmal, and Amin, Faiz Ul
- Subjects
POLYMYXIN B ,PSEUDOMONAS aeruginosa ,SUPPURATION ,MICROPLATES ,CHEMICAL reduction ,POLYMYXIN ,SILVER nanoparticles - Abstract
Pseudomonas aeruginosa (P. aeruginosa) is an aerobic gram-negative, non-spore forming, rod-shaped bacterium. It accelerates the decline in lung function and ultimately leads to increased mortality and morbidity rate. Survival and virulence of P. aeruginosa is due to its biofilm formation ability. The main aim of this study was to test the synergistic effect of silver nanoparticles (AgNPs) in combination with Polymyxin B against biofilms of P. aeruginosa. A total of 500 pus aspirations were collected and bacterial pathogens were identified. Biofilm formation was attained using a glass tube method and microtiter plate assay. The minimum inhibitory concentration of Polymyxin B was determined using agar well diffusion method. Silver nanoparticles were synthesized by chemical reduction method followed by determination of their anti-pseudomonal ability separately and in combination with Polymyxin B using microtiter plate assay. Our results showed that 120 out of 500 samples were Pseudomonas positive. The ratio of multidrug-resistant (MDR) in our collected Pseudomonas samples was 83% (25/30). Generally, the minimum inhibitory concentration (MIC) of Polymyxin B was 16 µg/mL and that of AgNPs was null. However, AgNPs showed great synergistic effect in combination with Polymyxin B. Synergistically, the efficacy of Polymyxin B was enhanced four times as compared to unaided Polymyxin B. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
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8. A Novel Magnetic Actuation Scheme to Disaggregate Nanoparticles and Enhance Passage across the Blood--Brain Barrier.
- Author
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Hoshiar, Ali Kafash, Le, Tuan-Anh, Amin, Faiz Ul, Kim, Myeong Ok, and Yoon, Jungwon
- Subjects
BLOOD-brain barrier ,DRUG delivery systems ,MAGNETIC nanoparticles - Abstract
The blood--brain barrier (BBB) hinders drug delivery to the brain. Despite various efforts to develop preprogramed actuation schemes for magnetic drug delivery, the unmodeled aggregation phenomenon limits drug delivery performance. This paper proposes a novel scheme with an aggregation model for a feed-forward magnetic actuation design. A simulation platform for aggregated particle delivery is developed and an actuation scheme is proposed to deliver aggregated magnetic nanoparticles (MNPs) using a discontinuous asymmetrical magnetic actuation. The experimental results with a Y-shaped channel indicated the success of the proposed scheme in steering and disaggregation. The delivery performance of the developed scheme was examined using a realistic, three-dimensional (3D) vessel simulation. Furthermore, the proposed scheme enhanced the transport and uptake of MNPs across the BBB in mice. The scheme presented here facilitates the passage of particles across the BBB to the brain using an electromagnetic actuation scheme. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
9. Osmotin-loaded magnetic nanoparticles with electromagnetic guidance for the treatment of Alzheimer's disease.
- Author
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Amin, Faiz Ul, Hoshiar, Ali Kafash, Do, Ton Duc, Noh, Yeongil, Shah, Shahid Ali, Khan, Muhammad Sohail, Yoon, Jungwon, and Kim, Myeong Ok
- Published
- 2017
- Full Text
- View/download PDF
10. Functionalized Magnetic Force Enhances Magnetic Nanoparticle Guidance: From Simulation to Crossing of the Blood–Brain Barrier In Vivo.
- Author
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Do, Ton Duc, Amin, Faiz Ul, Noh, Yeongil, Kim, Myeong Ok, and Yoon, Jungwon
- Subjects
- *
MAGNETISM , *MAGNETIC nanoparticles , *SIMULATION methods & models , *BLOOD-brain barrier , *MAGNETIC particles , *ELECTROMAGNETIC actuators - Abstract
In recent studies, we introduced the concept of functionalized magnetic force as a method to prevent nanoparticles from sticking to vessel walls caused by extensive simulation and in vitro experiments involving a Y-shaped channel. In this paper, we further investigated the effectiveness of the functionalized magnetic force with a realistic 3-D vessel through simulations. For the simulations, we considered a more realistic continuous injection of particles with different magnetic forces and frequencies. Based on the results from our simulation studies, we performed in vivo mice experiments to evaluate the effectiveness of using a functionalized magnetic force to aid magnetic nanoparticles (MNPs) in crossing the blood–brain barrier (BBB). To implement the functionalized magnetic force, we developed an electromagnetic actuator regulated by a programmable direct current power supply. Our results indicate that a functionalized magnetic field (FMF) can effectively prevent MNPs from sticking, and also guide them across the BBB. We used 770 nm fluorescent carboxyl MNPs in this paper. Following intravenous administration of MNPs into mice, we applied an external magnetic field to mediate transport of the MNPs across the BBB and into the brain. Furthermore, we evaluated the differential effects of FMFs (0.25, 0.5, and 1 Hz) and constant magnetic fields (CMFs) on the transport of MNPs across the BBB. Our results showed that an FMF is more effective than a CMF in the transport and uptake of MNPs across the BBB in mice. In particular, applying an FMF with a 3 A current and 0.5 Hz frequency mediated the greatest transport and uptake of MNPs across the BBB in mice. [ABSTRACT FROM PUBLISHER]
- Published
- 2016
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- View/download PDF
11. Nanoscale-alumina induces oxidative stress and accelerates amyloid beta (Aβ) production in ICR female mice.
- Author
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Shah, Shahid Ali, Yoon, Gwang Ho, Ahmad, Ashfaq, Ullah, Faheem, Amin, Faiz Ul, and Kim, Myeong Ok
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- 2015
- Full Text
- View/download PDF
12. Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice.
- Author
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Amin, Faiz Ul, Shah, Shahid Ali, and Kim, Myeong Ok
- Abstract
Increasing evidence demonstrates that β-amyloid (Aβ) elicits oxidative stress, which contributes to the pathogenesis and disease progression of Alzheimer's disease (AD). The aims of the present study were to determine and explore the antioxidant nature and potential mechanism of vanillic acid (VA) in Aβ1-42-induced oxidative stress and neuroinflammation mediated cognitive impairment in mice. An intracerebroventricular (i.c.v.) injection of Aβ1-42 into the mouse brain triggered increased reactive oxygen species (ROS) levels, neuroinflammation, synaptic deficits, memory impairment, and neurodegeneration. In contrast, the i.p. (intraperitoneal) administration of VA (30 mg/kg, for 3 weeks) after Aβ1-42-injection enhanced glutathione levels (GSH) and abrogated ROS generation accompanied by an induction of the endogenous nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) via the activation of Akt and glycogen synthase kinase 3β (GSK-3β) in the brain mice. Additionally, VA treatment decreased Aβ1-42-induced neuronal apoptosis and neuroinflammation and improved synaptic and cognitive deficits. Moreover, VA was nontoxic to HT22 cells and increased cell viability after Aβ1-42 exposure. To our knowledge, this study is the first to reveal the neuroprotective effect of VA against Aβ1-42-induced neurotoxicity. Our findings demonstrate that VA could potentially serve as a novel, promising, and accessible neuroprotective agent against progressive neurodegenerative diseases such as AD. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
13. Studies of aggregated nanoparticles steering during magnetic-guided drug delivery in the blood vessels.
- Author
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Hoshiar, Ali Kafash, Le, Tuan-Anh, Amin, Faiz Ul, Kim, Myeong Ok, and Yoon, Jungwon
- Subjects
- *
MAGNETIC fields , *ELECTROMAGNETISM , *TARGETED drug delivery , *BLOOD vessels , *CLUSTERING of particles , *NANOPARTICLES - Abstract
Magnetic-guided targeted drug delivery (TDD) systems can enhance the treatment of diverse diseases. Despite the potential and promising results of nanoparticles, aggregation prevents precise particle guidance in the vasculature. In this study, we developed a simulation platform to investigate aggregation during steering of nanoparticles using a magnetic field function. The magnetic field function (MFF) comprises a positive and negative pulsed magnetic field generated by electromagnetic coils, which prevents adherence of particles to the vessel wall during magnetic guidance. A commonly used Y-shaped vessel was simulated and the performance of the MFF analyzed; the experimental data were in agreement with the simulation results. Moreover, the effects of various parameters on magnetic guidance were evaluated and the most influential identified. The simulation results presented herein will facilitate more precise guidance of nanoparticles in vivo. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
14. The identification of a Distinct Astrocyte Subtype that Diminishes in Alzheimer's Disease.
- Author
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Wei H, Withrow J, Rakshit J, Amin FU, Nahm J, Mowry FE, Mao Z, Bhattacharjee MB, Zhu JJ, Yang Y, and Wu JQ
- Abstract
Alzheimer's disease (AD) is characterized by the presence of two hallmark pathologies: the accumulation of Amyloid beta (Aβ) and tau proteins in the brain. There is a growing body of evidence suggesting that astrocytes, a type of glial cell in the brain, play crucial roles in clearing Aβ and binding to tau proteins. However, due to the heterogeneity of astrocytes, the specific roles of different astrocyte subpopulations in response to Aβ and tau remain unclear. To enhance the understanding of astrocyte subpopulations in AD, we investigated astrocyte lineage cells based on single-nuclei transcriptomic data obtained from both human and mouse samples. We characterized the diversity of astrocytes and identified global and subpopulation-specific transcriptomic changes between control and AD samples. Our findings revealed the existence of a specific astrocyte subpopulation marked by low levels of GFAP and the presence of AQP4 and CD63 expression, which showed functional enrichment in Aβ clearance and tau protein binding, and diminished in AD. We verified this type of astrocytes in mouse models and in AD patient brain samples. Furthermore, our research also unveiled significant alterations of the ligand-receptor interactions between astrocytes and other cell types. These changes underscore the complex interplay between astrocytes and neighboring cells in the context of AD. Overall, our work gives insights into astrocyte heterogeneity in the context of AD and reveals a distinct astrocyte subpopulation that holds potential for therapeutic interventions in AD. Targeting specific astrocyte subpopulations may offer new avenues for the development of novel treatments for AD.
- Published
- 2024
- Full Text
- View/download PDF
15. A Novel Magnetic Actuation Scheme to Disaggregate Nanoparticles and Enhance Passage across the Blood-Brain Barrier.
- Author
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Hoshiar AK, Le TA, Amin FU, Kim MO, and Yoon J
- Abstract
The blood-brain barrier (BBB) hinders drug delivery to the brain. Despite various efforts to develop preprogramed actuation schemes for magnetic drug delivery, the unmodeled aggregation phenomenon limits drug delivery performance. This paper proposes a novel scheme with an aggregation model for a feed-forward magnetic actuation design. A simulation platform for aggregated particle delivery is developed and an actuation scheme is proposed to deliver aggregated magnetic nanoparticles (MNPs) using a discontinuous asymmetrical magnetic actuation. The experimental results with a Y-shaped channel indicated the success of the proposed scheme in steering and disaggregation. The delivery performance of the developed scheme was examined using a realistic, three-dimensional (3D) vessel simulation. Furthermore, the proposed scheme enhanced the transport and uptake of MNPs across the BBB in mice. The scheme presented here facilitates the passage of particles across the BBB to the brain using an electromagnetic actuation scheme., Competing Interests: The authors declare no conflict of interest.
- Published
- 2017
- Full Text
- View/download PDF
16. Functionalized electromagnetic actuation method for aggregated nanoparticles steering.
- Author
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Hoshiar AK, Tuan-Anh Le, Amin FU, Myeong Ok Kim, and Jungwon Yoon
- Subjects
- Drug Delivery Systems, Electromagnetic Phenomena, Magnetics, Magnetite Nanoparticles
- Abstract
Despite the promising results in magnetic nanoparticles (MNPs) based targeted drug delivery (TDD), the aggregation of the magnetic nanoparticles deteriorates targeting performance. This paper aims to introduce a magnetic actuation function for aggregated nanoparticles steering in vascular network. To improve the drug delivery performance, first the governing dynamics has been introduced, next the modified field function (MFF) concept has been proposed and finally a computational platform for a Y-shape channel has been used to simulate the particles steering performance. The results showed an acceptable agreement with the experimental results. The proposed actuation method enables us to more accurately steer aggregated nanoparticles and improves targeting performance.
- Published
- 2017
- Full Text
- View/download PDF
17. Anthocyanins encapsulated by PLGA@PEG nanoparticles potentially improved its free radical scavenging capabilities via p38/JNK pathway against Aβ 1-42 -induced oxidative stress.
- Author
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Amin FU, Shah SA, Badshah H, Khan M, and Kim MO
- Subjects
- Alzheimer Disease prevention & control, Amyloid beta-Peptides pharmacology, Biological Availability, Cell Culture Techniques, Cell Line, Cell Survival, Drug Delivery Systems, Drug Liberation, Humans, Microscopy, Electron, Transmission, Neuroprotective Agents pharmacology, Oxidative Stress, Particle Size, Peptide Fragments pharmacology, Polyethylene Glycols chemistry, Polylactic Acid-Polyglycolic Acid Copolymer, Anthocyanins pharmacology, Free Radical Scavengers pharmacology, Lactic Acid chemistry, MAP Kinase Signaling System, Nanoparticles chemistry, Polyglycolic Acid chemistry
- Abstract
Background: In order to increase the bioavailability of hydrophilic unstable drugs like anthocyanins, we employed a polymer-based nanoparticles approach due to its unique properties such as high stability, improved bioavailability and high water-soluble drug loading efficiency. Anthocyanins constitute a subfamily of flavonoids that possess anti-oxidative, anti-inflammatory and neuroprotective properties. However, anthocyanins are unstable because their phenolic hydroxyl groups are easily oxidized into quinones, causing a reduced biological activity. To overcome this drawback and improve the free radical scavenging capabilities of anthocyanins, in the current study we for the first time encapsulated the anthocyanins in biodegradable nanoparticle formulation based on poly (lactide-co-glycolide) (PLGA) and a stabilizer polyethylene glycol (PEG)-2000. The biological activity and neuroprotective effect of anthocyanin loaded nanoparticles (An-NPs) were investigated in SH-SY5Y cell lines., Results: Morphological examination under transmission electron microscopy (TEM) showed the formation of smooth spherically shaped nanoparticles. The average particle size and zeta potential of An-NPs were in the range of 120-165 nm and -12 mV respectively, with a low polydispersity index (0.4) and displayed a biphasic release profile in vitro. Anthocyanins encapsulation in PLGA@PEG nanoparticles (NPs) did not destroy its inherent properties and exhibit more potent neuroprotective properties. An-NPs were nontoxic to SH-SY5Y cells and increased their cell viability against Aβ
1-42 by its free radical scavenging characteristics and abrogated ROS generation via the p38-MAPK/JNK pathways accompanied by induction of endogenous nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1). Comparative to native bulk anthocyanins, An-NPs effectively attenuated Alzheimer's markers like APP (amyloid precursor protein), BACE-1 (beta-site amyloid precursor protein cleaving enzyme 1), neuroinflammatory markers such as p-NF-kB (phospho-nuclear factor kappa B), TNF-α (tumor necrosis factor) and iNOS (inducible nitric oxide synthase) and neuroapoptotic markers including Bax, Bcl2 , and Caspase-3 protein expressions accompanied by neurodegeneration against Aβ1-42 in SH-SY5Y cell lines., Conclusions: Overall, this data not only confirmed the therapeutic potential of anthocyanins in reducing AD pathology but also offer an effective way to improve the efficiency of anthocyanins through the use of nanodrug delivery systems.- Published
- 2017
- Full Text
- View/download PDF
18. Vanillic acid attenuates Aβ 1-42 -induced oxidative stress and cognitive impairment in mice.
- Author
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Amin FU, Shah SA, and Kim MO
- Subjects
- Alzheimer Disease metabolism, Alzheimer Disease pathology, Amyloid Precursor Protein Secretases genetics, Amyloid Precursor Protein Secretases metabolism, Animals, Apoptosis drug effects, Aspartic Acid Endopeptidases genetics, Aspartic Acid Endopeptidases metabolism, Astrocytes drug effects, Astrocytes metabolism, Cell Line, Glycogen Synthase Kinase 3 beta metabolism, Memory Disorders, Mice, Microglia drug effects, Microglia metabolism, NF-E2-Related Factor 2 metabolism, Neurons drug effects, Neurons metabolism, Neuroprotective Agents pharmacology, Protein Aggregates, Protein Aggregation, Pathological, Proteolysis, Proto-Oncogene Proteins c-akt metabolism, Reactive Oxygen Species metabolism, Signal Transduction drug effects, Amyloid beta-Peptides pharmacology, Cognitive Dysfunction drug therapy, Oxidative Stress drug effects, Vanillic Acid pharmacology
- Abstract
Increasing evidence demonstrates that β-amyloid (Aβ) elicits oxidative stress, which contributes to the pathogenesis and disease progression of Alzheimer's disease (AD). The aims of the present study were to determine and explore the antioxidant nature and potential mechanism of vanillic acid (VA) in Aβ
1-42 -induced oxidative stress and neuroinflammation mediated cognitive impairment in mice. An intracerebroventricular (i.c.v.) injection of Aβ1-42 into the mouse brain triggered increased reactive oxygen species (ROS) levels, neuroinflammation, synaptic deficits, memory impairment, and neurodegeneration. In contrast, the i.p. (intraperitoneal) administration of VA (30 mg/kg, for 3 weeks) after Aβ1-42 -injection enhanced glutathione levels (GSH) and abrogated ROS generation accompanied by an induction of the endogenous nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) via the activation of Akt and glycogen synthase kinase 3β (GSK-3β) in the brain mice. Additionally, VA treatment decreased Aβ1-42 -induced neuronal apoptosis and neuroinflammation and improved synaptic and cognitive deficits. Moreover, VA was nontoxic to HT22 cells and increased cell viability after Aβ1-42 exposure. To our knowledge, this study is the first to reveal the neuroprotective effect of VA against Aβ1-42 -induced neurotoxicity. Our findings demonstrate that VA could potentially serve as a novel, promising, and accessible neuroprotective agent against progressive neurodegenerative diseases such as AD.- Published
- 2017
- Full Text
- View/download PDF
19. Anthocyanins abrogate glutamate-induced AMPK activation, oxidative stress, neuroinflammation, and neurodegeneration in postnatal rat brain.
- Author
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Shah SA, Amin FU, Khan M, Abid MN, Rehman SU, Kim TH, Kim MW, and Kim MO
- Subjects
- AMP-Activated Protein Kinases genetics, Animals, Animals, Newborn, Antioxidants pharmacology, Antioxidants therapeutic use, Cell Line, Transformed, Cyclooxygenase 2 metabolism, Encephalitis chemically induced, Enzyme Activation drug effects, Gene Expression Regulation, Developmental drug effects, Glutamine toxicity, Humans, Nerve Degeneration chemically induced, Neuroblastoma pathology, RNA, Small Interfering genetics, RNA, Small Interfering metabolism, Rats, Rats, Sprague-Dawley, Reactive Oxygen Species metabolism, Signal Transduction drug effects, AMP-Activated Protein Kinases metabolism, Anthocyanins pharmacology, Anthocyanins therapeutic use, Encephalitis drug therapy, Nerve Degeneration drug therapy, Oxidative Stress drug effects
- Abstract
Background: Glutamate-induced excitotoxicity, oxidative damage, and neuroinflammation are believed to play an important role in the development of a number of CNS disorders. We recently reported that a high dose of glutamate could induce AMPK-mediated neurodegeneration in the postnatal day 7 (PND7) rat brain. Yet, the mechanism of glutamate-induced oxidative stress and neuroinflammation in the postnatal brain is not well understood. Here, we report for the first time the mechanism of glutamate-induced oxidative damage, neuroinflammation, and neuroprotection by polyphenolic anthocyanins in PND7., Methods: PND7 rat brains, SH-SY5Y, and BV2 cells treated either alone with glutamate or in combination with anthocyanins and compound C were examined with Western blot and immunofluorescence techniques. Additionally, reactive oxygen species (ROS) assay and other ELISA kit assays were employed to know the therapeutic efficacy of anthocyanins against glutamate., Results: A single injection of glutamate to developing rats significantly increased brain glutamate levels, activated and phosphorylated AMPK induction, and inhibited nuclear factor-E2-related factor 2 (Nrf2) after 2, 3, and 4 h in a time-dependent manner. In contrast, anthocyanin co-treatment significantly reduced glutamate-induced AMPK induction, ROS production, neuroinflammation, and neurodegeneration in the developing rat brain. Most importantly, anthocyanins increased glutathione (GSH and GSSG) levels and stimulated the endogenous antioxidant system, including Nrf2 and heme oxygenase-1 (HO-1), against glutamate-induced oxidative stress. Interestingly, blocking AMPK with compound C in young rats abolished glutamate-induced neurotoxicity. Similarly, all these experiments were replicated in SH-SY5Y cells by silencing AMPK with siRNA, which suggests that AMPK is the key mediator in glutamate-induced neurotoxicity., Conclusions: Here, we report for the first time that anthocyanins can potentially decrease glutamate-induced neurotoxicity in young rats. Our work demonstrates that glutamate is toxic to the developing rat brain and that anthocyanins can minimize the severity of glutamate-induced neurotoxicity in an AMPK-dependent manner.
- Published
- 2016
- Full Text
- View/download PDF
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