D-Galactose-Induced Accelerated Aging Model on Auditory Cortical Neurons by Regulating Oxidative Stress and Apoptosis in Vitro

2021 ◽  
Author(s):  
C. Zhao ◽  
Z. Chen ◽  
W. Liang ◽  
Z. Yang ◽  
Zhengde Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Accelerated Aging ◽  
Aging Model

scholarly journals Neurotherapeutic Effect of Inula britannica var. Chinensis against H2O2-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Jin Young Hong ◽  
Hyunseong Kim ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cortical Neurons ◽  
Inflammatory Diseases ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Inula Britannica ◽  
Oxidative Effects

Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.

Low level laser therapy reduces oxidative stress in cortical neurons in vitro

2012 ◽  
Author(s):  
Ying-Ying Huang ◽  
Clark E. Tedford ◽  
Thomas McCarthy ◽  
Michael R. Hamblin
Keyword(s):  
Oxidative Stress ◽  
Laser Therapy ◽  
Cortical Neurons ◽  
Low Level Laser Therapy ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser

scholarly journals d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model

2020 ◽  
Vol 21 (3) ◽  
pp. 311-323 ◽  
Author(s):  
Bin Guo ◽  
Qing Guo ◽  
Zhan Wang ◽  
Jian-Bo Shao ◽  
Ke Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Basilar Membrane ◽  
Aging Model ◽  
In Vitro Aging

scholarly journals Upregulation of Peroxiredoxin 3 Protects Afg3l2-KO Cortical Neurons In Vitro from Oxidative Stress: A Paradigm for Neuronal Cell Survival under Neurodegenerative Conditions

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Barbara Bettegazzi ◽  
Ilaria Pelizzoni ◽  
Floramarida Salerno Scarzella ◽  
Lisa Michelle Restelli ◽  
Daniele Zacchetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Mitochondrial Dynamics ◽  
Neuronal Cell ◽  
The Other ◽  
Antioxidant Defenses ◽  
Glutathione Depletion ◽  
Other Hand ◽  
Peroxiredoxin 3

Several neurodegenerative disorders exhibit selective vulnerability, with subsets of neurons more affected than others, possibly because of the high expression of an altered gene or the presence of particular features that make them more susceptible to insults. On the other hand, resilient neurons may display the ability to develop antioxidant defenses, particularly in diseases of mitochondrial origin, where oxidative stress might contribute to the neurodegenerative process. In this work, we investigated the oxidative stress response of embryonic fibroblasts and cortical neurons obtained from Afg3l2-KO mice. AFG3L2 encodes a subunit of a protease complex that is expressed in mitochondria and acts as both quality control and regulatory enzyme affecting respiration and mitochondrial dynamics. When cells were subjected to an acute oxidative stress protocol, the survival of AFG3L2-KO MEFs was not significantly influenced and was comparable to that of WT; however, the basal level of the antioxidant molecule glutathione was higher. Indeed, glutathione depletion strongly affected the viability of KO, but not of WT MEF, thereby indicating that oxidative stress is more elevated in KO MEF even though well controlled by glutathione. On the other hand, when cortical KO neurons were put in culture, they immediately appeared more vulnerable than WT to the acute oxidative stress condition, but after few days in vitro, the situation was reversed with KO neurons being more resistant than WT to acute stress. This compensatory, protective competence was not due to the upregulation of glutathione, rather of two mitochondrial antioxidant proteins: superoxide dismutase 2 and, at an even higher level, peroxiredoxin 3. This body of evidence sheds light on the capability of neurons to activate neuroprotective pathways and points the attention to peroxiredoxin 3, an antioxidant enzyme that might be critical for neuronal survival also in other disorders affecting mitochondria.

scholarly journals Oxidative Stress Induces Disruption of the Axon Initial Segment

ASN NEURO ◽  
2017 ◽  
Vol 9 (6) ◽  
pp. 175909141774542 ◽  
Author(s):  
Kareem C. Clark ◽  
Brooke A. Sword ◽  
Jeffrey L. Dupree
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Cortical Neurons ◽  
Initial Segment ◽  
Reactive Oxygen ◽  
Axon Initial Segment ◽  
Voltage Dependent ◽  
Reversible Loss

The axon initial segment (AIS), the domain responsible for action potential initiation and maintenance of neuronal polarity, is targeted for disruption in a variety of central nervous system pathological insults. Previous work in our laboratory implicates oxidative stress as a potential mediator of structural AIS alterations in two separate mouse models of central nervous system inflammation, as these effects were attenuated following reactive oxygen species scavenging and NADPH oxidase-2 ablation. While these studies suggest a role for oxidative stress in modulation of the AIS, the direct effects of reactive oxygen and nitrogen species (ROS/RNS) on the stability of this domain remain unclear. Here, we demonstrate that oxidative stress, as induced through treatment with 3-morpholinosydnonimine (SIN-1), a spontaneous ROS/RNS generator, drives a reversible loss of AIS protein clustering in primary cortical neurons in vitro. Pharmacological inhibition of both voltage-dependent and intracellular calcium (Ca2+) channels suggests that this mechanism of AIS disruption involves Ca2+ entry specifically through L-type voltage-dependent Ca2+ channels and its release from IP3-gated intracellular stores. Furthermore, ROS/RNS-induced AIS disruption is dependent upon activation of calpain, a Ca2+-activated protease previously shown to drive AIS modulation. Overall, we demonstrate for the first time that oxidative stress, as induced through exogenously applied ROS/RNS, is capable of driving structural alterations in the AIS complex.

scholarly journals Low-level laser therapy (LLLT) reduces oxidative stress in primary cortical neurons in vitro

2012 ◽  
pp. n/a-n/a ◽  
Author(s):  
Ying-Ying Huang ◽  
Kazuya Nagata ◽  
Clark E. Tedford ◽  
Thomas McCarthy ◽  
Michael R. Hamblin
Keyword(s):  
Oxidative Stress ◽  
Laser Therapy ◽  
Cortical Neurons ◽  
Low Level Laser Therapy ◽  
Primary Cortical Neurons ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser

scholarly journals Characterization of Parylene-C degradation mechanisms: In vitro reactive accelerated aging model compared to multiyear in vivo implantation

Biomaterials ◽  
2020 ◽  
Vol 232 ◽  
pp. 119731 ◽  
Author(s):  
Ryan Caldwell ◽  
Matthew G. Street ◽  
Rohit Sharma ◽  
Pavel Takmakov ◽  
Brian Baker ◽  
...  
Keyword(s):  
Accelerated Aging ◽  
Degradation Mechanisms ◽  
Parylene C ◽  
Aging Model

Sestrin2 protects against traumatic brain injury by reinforcing the activation of Nrf2 signaling

2020 ◽  
pp. 096032712098422
Author(s):  
Xiaobin Liu ◽  
Min Li ◽  
Jiabao Zhu ◽  
Weidong Huang ◽  
Jinning Song
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cortical Neurons ◽  
In Vitro Models ◽  
Related Factor ◽  
Neuroprotective Effects ◽  
Nuclear Levels

Sestrin2 (SESN2) is stress-inducible protein that confers cytoprotective effects against various noxious stimuli. Accumulating evidence has documented that SESN2 has potent anti-apoptosis and anti-oxidative stress functions. However, whether it provides neuroprotection in traumatic brain injury (TBI) models remains unexplored. The purpose of this study was to explore the regulatory effect of SESN2 on TBI using in vivo and in vitro models. We found that TBI resulted in a marked induction of SESN2 in the cerebral cortex tissues of mice. SESN2 overexpression in the brain by in vivo gene transfer significantly decreased neurological deficit, brain edema, and neuronal apoptosis of mice with TBI. Moreover, the overexpression of SESN2 significantly decreased the oxidative stress induced by TBI in mice. In vitro studies of TBI demonstrated that SESN2 overexpression decreased apoptosis and oxidative stress in scratch-injured cortical neurons. Notably, SESN2 overexpression increased the nuclear levels of nuclear factor-erythroid 2-related factor 2 (Nrf2) and enhanced the activation of Nrf2 antioxidant signaling in in vivo and in vitro models of TBI. In addition, the inhibition of Nrf2 significantly abolished SESN2-mediated neuroprotective effects in vivo and in vitro. In conclusion, these results of our work demonstrate that SESN2 protects against TBI by enhancing the activation of Nrf2 antioxidant signaling.

Sign in / Sign up

Export Citation Format

Share Document