Antioxidant Properties and Protective Effects of Aerial Parts from Cnidium officinale Makino on Oxidative Stress-Induced Neuronal Cell Death

1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ) has previously been found to have effective anti-oxidant and anti-lipid-peroxidative activity. We aimed to elucidate whether HTHQ can prevent dopaminergic neuronal cell death by investigating the effect on l-DOPA-induced cytotoxicity in PC12 cells. HTHQ protected from both l-DOPA-induced cell death and superoxide dismutase activity reduction. When assessing the effect of HTHQ on oxidative stress-related signaling pathways, HTHQ inhibited l-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). HTHQ also normalized l-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival. Taken together, HTHQ exhibits protective effects against l-DOPA-induced cell death through modulation of the ERK1/2-p38MAPK-JNK1/2-Bad-Bax signaling pathway in PC12 cells. These results suggest that HTHQ may show ameliorative effects against oxidative stress-induced dopaminergic neuronal cell death, although further studies in animal models of Parkinson’s disease are required to confirm this.

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Momordica charantia Ethanol Extract Attenuates H2O2-Induced Cell Death by Its Antioxidant and Anti-Apoptotic Properties in Human Neuroblastoma SK-N-MC Cells

Nutrients ◽

10.3390/nu10101368 ◽

2018 ◽

Vol 10 (10) ◽

pp. 1368 ◽

Cited By ~ 5

Author(s):

Kkot Kim ◽

SeonAh Lee ◽

Inhae Kang ◽

Jung-Hee Kim

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Ethanol Extract ◽

Momordica Charantia ◽

Mitogen Activated Protein Kinase ◽

Cellular Damage ◽

Protective Effects ◽

Human Neuroblastoma

Oxidative stress, which is induced by reactive oxygen species (ROS), causes cellular damage which contributes to the pathogenesis of neurodegenerative diseases. Momordica charantia (MC), a traditional medicinal plant, is known to have a variety of health benefits, such as antidiabetic, anti-inflammatory, and antioxidant effects. However, it is unknown whether MC has protective effects against oxidative stress-induced neuronal cell death. The aim of this study was to investigate the potential action of MC on oxidative stress induced by H2O2. First, we tested whether the pretreatment of Momordica charantia ethanol extract (MCEE) attenuates H2O2-induced cell death in human neuroblastoma SK-N-MC cells. MCEE pretreatment significantly improved cell viability and apoptosis that deteriorated by H2O2. Further, MCEE ameliorated the imbalance between intracellular ROS production and removal through the enhancement of the intracellular antioxidant system. Intriguingly, the inhibition of apoptosis was followed by the blockage of mitochondria-dependent cell death cascades and suppression of the phosphorylation of the mitogen-activated protein kinase signaling (MAPKs) pathway by MCEE. Taken together, MCEE was shown to be effective in protecting against H2O2-induced cell death through its antioxidant and anti-apoptotic properties.

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Protective effects of transduced PEP-1-Frataxin protein on oxidative stress-induced neuronal cell death

Journal of the Neurological Sciences ◽

10.1016/j.jns.2010.08.016 ◽

2010 ◽

Vol 298 (1-2) ◽

pp. 64-69 ◽

Cited By ~ 7

Author(s):

Mi Jin Kim ◽

Dae Won Kim ◽

Ki-Yeon Yoo ◽

Eun Jeong Sohn ◽

Hoon Jae Jeong ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Protective Effects

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An Insight of Vitamin E as Neuroprotective Agents

Progress In Microbes & Molecular Biology ◽

10.36877/pmmb.a0000071 ◽

2020 ◽

Vol 3 (1) ◽

Author(s):

Hui-Min Yap ◽

Kwan-Liang Lye

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Vitamin E ◽

Neuronal Cell Death ◽

Antioxidant Properties ◽

Radical Scavenging ◽

Neuronal Cell ◽

Redox Balance ◽

The Body ◽

Neuroprotective Effects

Nervous system is the network of nerve cells that transmits nerve impulses throughout the body. It is rich in both unsaturated fats and irons, making it predominantly susceptible to oxidative stress and damage. Oxidative stress reflects the disruption of the redox balance between the formation and clearance of highly free radicals, for instance reactive oxygen species (ROS) and reactive nitrogen species (RNS). Oxidative stress will further damage the cell lipid, protein and DNA. Oxidative stress has a role in the modulation of critical cellular functions, such as apoptosis program activation, ion transport and calcium mobilization which lead to cell death. Many studies were conducted to prevent neuronal cell death caused by oxidative stress through administration of free radical scavenging antioxidant, such as vitamin E. Vitamin E is known as a chain-breaking antioxidant that showed the capability to increase the viability of neuronal cells that had undergone glutamate injury by inhibiting glutamate-induced pp60 (c-Src) kinase activation. Vitamin E occurs in 8 forms, namely ?-, ?-, ?- and ?-tocopherols and ?-, ?-, ?-and ?-tocotrienols. Tocotrienols differ from tocopherols by possessing an unsaturated isoprenoid side chain instead of a saturated phytyl tail. Tocotrienols, compared to tocopherols, are lightly studied due to the abundance of ?-tocopherol in the human body and its antioxidant properties. Nevertheless, recent studies showed that ?-tocotrienol is more effective in preventing lipid peroxidation compared to ?-tocopherol. Furthermore, tocotrienol was discovered to protect neuronal cell through antioxidant-independent activities. The tocotrienol-rich fraction (TRF) is an extract that consists of 75% tocotrienol and 25% ?-tocopherol. TRF was reported to possess potent antioxidant, anti-inflammation, anticancer and cholesterol-lowering properties. Thus, this writing highlights the significant neuroprotective effects of tocotrienol and tocopherol.

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Protective Role of Transduced Tat-Thioredoxin1 (Trx1) against Oxidative Stress-Induced Neuronal Cell Death via ASK1-MAPK Signal Pathway

Biomolecules & Therapeutics ◽

10.4062/biomolther.2020.154 ◽

2021 ◽

Author(s):

Eun Ji Yeo ◽

Won Sik Eum ◽

Hyeon Ji Yeo ◽

Yeon Joo Choi ◽

Eun Jeong Sohn ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Protective Role ◽

Signal Pathway ◽

Mapk Signal Pathway

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Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽

10.3390/antiox10111702 ◽

2021 ◽

Vol 10 (11) ◽

pp. 1702

Author(s):

Sereen Sandouka ◽

Tawfeeq Shekh-Ahmad

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Status Epilepticus ◽

Temporal Lobe Epilepsy ◽

Antioxidant Capacity ◽

Temporal Lobe ◽

Epileptiform Activity ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

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Protective effects of cyclohexenone long chain alcohols against the neuronal cell death due to calcium overloading

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)48176-6 ◽

2000 ◽

Vol 82 ◽

pp. 178

Author(s):

Mihoko Hirata ◽

Remi Tsuchiya ◽

Miyuki Ogawa ◽

Nagisa Matsumoto ◽

Masashi Yamada ◽

...

Keyword(s):

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Protective Effects ◽

Calcium Overloading ◽

Long Chain

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Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells

Journal of Ginseng Research ◽

10.1016/j.jgr.2018.12.002 ◽

2019 ◽

Vol 43 (2) ◽

pp. 326-334 ◽

Cited By ~ 19

Author(s):

Dong Hoi Kim ◽

Dae Won Kim ◽

Bo Hyun Jung ◽

Jong Hun Lee ◽

Heesu Lee ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Ht22 Cells ◽

Ginsenoside Rb2

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Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

Molecules ◽

10.3390/molecules25010144 ◽

2019 ◽

Vol 25 (1) ◽

pp. 144 ◽

Cited By ~ 4

Author(s):

Chang-Hyun Park ◽

Ji Hoon Song ◽

Su-Nam Kim ◽

Ji Hwan Lee ◽

Hae-Jeung Lee ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Protein Kinases ◽

Apoptotic Cell ◽

Curcuma Longa ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Ht22 Cells ◽

Mitogen Activated Protein Kinases ◽

Mitogen Activated Protein

In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.

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