Seizure-Induced Oxidative Stress in Status Epilepticus: Is Antioxidant Beneficial?

Lin, Tsu-Kung; Chen, Shang-Der; Lin, Kai-Jung; Chuang, Yao-Chung

doi:10.3390/antiox9111029

Cited by 68 publications

(48 citation statements)

References 187 publications

(225 reference statements)

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“…Evidence has demonstrated that oxidative stress plays pivotal role in the pathophysiology of seizures. Researches have determined that antioxidants exerted anticonvulsant effects [17][18][19]. In line with aforementioned studies, our findings showed that Artemisia persica extract reduced the MDA levels and increased total antioxidant capacity in the serum and prefrontal cortex samples in PTZ-induced mice.…”

Section: Discussionsupporting

confidence: 90%

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NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

Boroujeni

Lorigooini

Piroti

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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It is necessary to seek more effective sources to design new drug against epilepsy. This study aimed to evaluate the effect of hydroalcoholic extract of Artemisia persica on pentylenetetrazole- (PTZ-) induced seizure in male mice by investigating the possible role of the NMDA receptor and antioxidative stress effect. The phenolic profile of A. persica extract was determined by HPLC-DAD analysis. Mice were treated with normal saline or A. persica extract or pentobarbital or a subeffective dose of extract plus ketamine (NMDA receptor antagonist) and/or effective dose of extract plus NMDA. PTZ (90 mg/kg) was injected intravenously for induction of seizure. The seizure threshold was measured. Then mice were euthanized and the antioxidant capacity and the level of malondialdehyde (MDA) of the prefrontal cortex and serum were measured. The gene expression of NMDA receptor subunits (Nr2a and Nr2b) was determined by real-time PCR. Findings showed that A. persica extract increased the seizure threshold, increased antioxidant capacity, and decreased MDA levels in the serum and brain samples. A. persica extract reduced the expression of NMDA receptor subunits. The result showed that ketamine potentiated the effect of the subeffective dose of extract. HPLC analysis showed that quercetin had the highest flavonoid content and also caffeic acid had the highest content of the phenolic acids. A. persica extract probably via NMDA receptor exerts anticonvulsant properties.

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Section: Discussionsupporting

confidence: 90%

“…Ample evidence demonstrated that mitochondrial dysfunction and oxidative stress play pivotal role in the pathophysiology of seizures. In this concept, research studies determined that antioxidants exerted anticonvulsant properties [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

Boroujeni

Lorigooini

Piroti

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Furthermore, since various cell models of epilepsy show a deficiency in coenzyme Q 10 (CoQ), supplementation of CoQ has been used as a treatment to alleviate pathophysiological disruptions. Importantly, CoQ supplementation has been shown to result in the enhancement of mitophagy flux via activation of AMPK, which in turn activates Silent Mating Type Information Regulation 2, S. Cerevisiae, Homolog 1 (SIRT1) and PGC-1α, leading to the induction of a metabolic stress resistance program that includes the induction of autophagy [ 205 ].…”

Section: Mitophagy In Neuropsychiatric and Neurodegenerative Diseasesmentioning

confidence: 99%

Mitophagy in Human Diseases

Doblado

Lueck

Rey

et al. 2021

IJMS

137

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Mitophagy is a selective autophagic process, essential for cellular homeostasis, that eliminates dysfunctional mitochondria. Activated by inner membrane depolarization, it plays an important role during development and is fundamental in highly differentiated post-mitotic cells that are highly dependent on aerobic metabolism, such as neurons, muscle cells, and hepatocytes. Both defective and excessive mitophagy have been proposed to contribute to age-related neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, metabolic diseases, vascular complications of diabetes, myocardial injury, muscle dystrophy, and liver disease, among others. Pharmacological or dietary interventions that restore mitophagy homeostasis and facilitate the elimination of irreversibly damaged mitochondria, thus, could serve as potential therapies in several chronic diseases. However, despite extraordinary advances in this field, mainly derived from in vitro and preclinical animal models, human applications based on the regulation of mitochondrial quality in patients have not yet been approved. In this review, we summarize the key selective mitochondrial autophagy pathways and their role in prevalent chronic human diseases and highlight the potential use of specific interventions.

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“…Iron is also abundant in the brain and is involved in the formation of hydroxyl radicals (Valko et al, 2007). Therefore, overproduction of oxidative stress in the brain leads to lipid peroxidation, epileptic activity, and neuronal death (Lin et al, 2020). Due to the essential role of oxidative stress and lipid peroxidation in inducing ferroptosis, these epileptic pathological processes in the brain are closely related to ferroptosis.…”

Section: Links Between Ferroptosis and Epilepsymentioning

confidence: 99%

Ferroptosis and Its Role in Epilepsy

Cai

Yang

2021

Front. Cell. Neurosci.

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Epilepsy is one of the most common symptoms of many neurological disorders. The typical excessive, synchronous and aberrant firing of neurons originating from different cerebral areas cause spontaneous recurrent epileptic seizures. Prolonged epilepsy can lead to neuronal damage and cell death. The mechanisms underlying epileptic pathogenesis and neuronal death remain unclear. Ferroptosis is a newly defined form of regulated cell death that is characterized by the overload of intracellular iron ions, leading to the accumulation of lethal lipid-based reactive oxygen species (ROS). To date, studies have mainly focused on its role in tumors and various neurological disorders, including epilepsy. Current research shows that inhibition of ferroptosis is likely to be an effective therapeutic approach for epilepsy. In this review, we outline the pathogenesis of ferroptosis, regulatory mechanisms of ferroptosis, related regulatory molecules, and their effects on epilepsy, providing a new direction for discovering new therapeutic targets in epilepsy.

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Seizure-Induced Oxidative Stress in Status Epilepticus: Is Antioxidant Beneficial?

Cited by 68 publications

References 187 publications

NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

Mitophagy in Human Diseases

Ferroptosis and Its Role in Epilepsy

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