A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells

Li, Xin; Xu, Haoxiang; Tao, Ling; Yang, Yuefan; Jing, Da; Dai, Shuhui; Luo, Peng; Qian, Xu

doi:10.3389/fnins.2017.00042

Cited by 14 publications

(14 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The reaction was stopped by adding 0.4 mol/l of NaOH. Activity of LDH was calculated from absorbance at 440 nm, and the background absorbance from the culture medium that was not used for cell culture was subtracted from all absorbance measurements ( 22 , 23 ).…”

Section: Methodsmentioning

confidence: 99%

Leptin Maintained Zinc Homeostasis Against Glutamate-Induced Excitotoxicity by Preventing Mitophagy-Mediated Mitochondrial Activation in HT22 Hippocampal Neuronal Cells

Jin

Hóng

2018

Front. Neurol.

View full text Add to dashboard Cite

Developmental seizure-induced long-term neuronal hyperexcitation is partially mediated by regenerative mossy fiber sprouting in hippocampus. Yet, there are no effective drugs available to block this pathological process. Recently, leptin has been shown to prevent the sprouting of hippocampal mossy fibers and abnormalities in the neurobehavioral parameters. However, their underlying molecular mechanisms are largely unknown. The purpose of this study was to determine the effect of glutamate on the parameters of zinc homeostasis, mitochondrial functions, and mitophagy regulating factors, as well as to investigate the protective effects of leptin against cytotoxicity of glutamate in murine HT22 hippocampal neuronal cells. Cells were assigned to one of the four groups as follows: control group, leptin alone group, glutamate injury group, and leptin pretreatment group. Our results demonstrated that glutamate induced a decrease in superoxide dismutase, GSH (glutathione), and mitochondrial membrane potential and an increase in GSSG (oxidized glutathione), mitochondrial reactive oxygen species, and supplementation of leptin blocked the toxic effect of glutamate on cell survival. The glutamate-induced cytotoxicity was associated with an increase in mitophagy and intracellular zinc ion levels. Furthermore, glutamate activated the mitophagy markers PINK1, Parkin, and the ratio of LC3-II/LC3-I, as well as increased the expression of zinc transporter 3 (ZnT3). Leptin corrected these glutamate-caused alterations. Finally, the mitophagy inhibitor, CsA, significantly reduced intracellular zinc ion content and ZnT3 expression. These results suggest that mitophagy-mediated zinc dyshomeostasis and mitochondrial activation contributed to glutamate-induced HT22 neuronal cell injury and that leptin treatment could counteract these detrimental effects, thus highlighting mitophagy-mediated zinc homeostasis via mitochondrial activation as a potential strategy to counteract neuroexcitotoxicity.

show abstract

Section: Methodsmentioning

confidence: 99%

Leptin Maintained Zinc Homeostasis Against Glutamate-Induced Excitotoxicity by Preventing Mitophagy-Mediated Mitochondrial Activation in HT22 Hippocampal Neuronal Cells

Jin

Hóng

2018

Front. Neurol.

View full text Add to dashboard Cite

show abstract

“…The molecular ions were monitored at m/z 348.00/62.00 for AEA, m/z 379.10/287.10 for 2-AG, m/z 313.1/62.0 for C17:1 FAE, m/z 464. 4 Enzymatic assays. Tissue samples were cut into 200 µm thick sections and were homogenized in ice-cold Tris-HCl buffer (50 mM, pH 7.4) containing 0.32 M sucrose to obtain total proteins.…”

Section: Reverse Transcription-quantitative Pcr (Rt-qpcr) Analysismentioning

confidence: 99%

Endocannabinoid system and the expression of endogenous ceramides in human hepatocellular carcinoma

et al. 2019

View full text Add to dashboard Cite

The endogenous lipid metabolism network is associated with the occurrence and progression of malignancies. Endocannabinoids and ceramides have demonstrated their anti-proliferative and pro-apoptotic properties in a series of cancer studies. The aim of the present study was to evaluate the expression patterns of endocannabinoids and endogenous ceramides in 67 pairs of human hepatocellular carcinoma (HCC) tissues and non-cancerous counterpart controls. Anandamide (AEA), the major endocannabinoid, was reduced in tumor tissues, probably due to the high expression and activity of fatty acid amide hydrolase. Another important endocannabinoid, 2-arachidonylglycerol (2-AG), was elevated in tumor tissues compared with non-tumor controls, indicating that the biosynthesis of 2-AG is faster than the degradation of 2-AG in tumor cells. Furthermore, western blot analysis demonstrated that cannabinoid receptor 1 was downregulated, while cannabinoid receptor 2 was elevated in HCC tissues, in accordance with the alterations in the levels of AEA and 2-AG, respectively.

show abstract

“…In blue ( Duong and Kim, 2016 ), with a 1 mT/50 Hz SEMF. In green ( Luo and Xu, 2017 ), using a burst-modulated PEMF with a burst frequency of 15 Hz (burst width, 5 ms; burst wait, 60 ms) and 4.5 MHz carrying monophasic square signal. SMF: stationary magnetic field; PEMF: pulsed electromagnetic field; SEMF: sinusoidal electromagnetic field; MF: magnetic field; f : frequency; f P : pulse frequency; T P : pulse period; f C : carrying signal frequency; T C : carrying signal period; B Wd : burst width; B Wt : burst wait interval; T B : burst period; f B : burst frequency; f S : sinusoid frequency; T S : sinusoid period.…”

Section: Introductionmentioning

confidence: 99%

Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke

Gomez

Font

Brône

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

Cerebral stroke is a leading cause of death and adult-acquired disability worldwide. To this date, treatment options are limited; hence, the search for new therapeutic approaches continues. Electromagnetic fields (EMFs) affect a wide variety of biological processes and accumulating evidence shows their potential as a treatment for ischemic stroke. Based on their characteristics, they can be divided into stationary, pulsed, and sinusoidal EMF. The aim of this review is to provide an extensive literature overview ranging from in vitro to even clinical studies within the field of ischemic stroke of all EMF types. A thorough comparison between EMF types and their effects is provided, as well as an overview of the signal pathways activated in cell types relevant for ischemic stroke such as neurons, microglia, astrocytes, and endothelial cells. We also discuss which steps have to be taken to improve their therapeutic efficacy in the frame of the clinical translation of this promising therapy.

show abstract

A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells

Cited by 14 publications

References 28 publications

Leptin Maintained Zinc Homeostasis Against Glutamate-Induced Excitotoxicity by Preventing Mitophagy-Mediated Mitochondrial Activation in HT22 Hippocampal Neuronal Cells

Leptin Maintained Zinc Homeostasis Against Glutamate-Induced Excitotoxicity by Preventing Mitophagy-Mediated Mitochondrial Activation in HT22 Hippocampal Neuronal Cells

Endocannabinoid system and the expression of endogenous ceramides in human hepatocellular carcinoma

Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke

Contact Info

Product

Resources

About