Objective: To investigate the protective effects and its mechanisms of total epimedium flavonoids (TEF) against Quindinince acid (QA)-induced toxicity in SH-SY5Y cells.

Methods: The MT assay was used to detect the toxicity of QA and the cell viability of pretreatment of TEF and co-incubation with QA in SH-SY5Y cells; Cell apoptosis was observed by Hochest33258 staining; SOD and GSH-Px activities as well as MDA content were measured by colorimetric method; The mitochondrial membrane potential (delta psi m) and intracellular free calcium concentration ([Ca2+]i) were monitored by FCM.

Results: TEF increased the cell viability of SH-SY5Y cells, reduced apoptosis cells significantly, improved SOD and GSH-Px activities, decreased MDA content, increased the mitochondrial membrane potential and reduced intracellular free calcium concentration( [Ca2+]i ).

Conclusion: TEF has significant protective effects against QA-induced toxicity in SH-SY5Y cells,the action mechanism may be associated with resisting oxidative stress, decreasing the [Ca2]i and up-regulating delta psi m.

Download full-text PDF

Source

Publication Analysis

Top Keywords

qa-induced toxicity
12
toxicity sh-sy5y
12
total epimedium
8
epimedium flavonoids
8
protective effects
8
cell viability
8
sh-sy5y cells
8
sod gsh-px
8
gsh-px activities
8
mda content
8

Similar Publications

Objective: Increased quinolinic acid (QA) accumulation has been found in many neurodegenerative diseases. Artemisia absinthium (A. absinthium) has been reported to have neuroprotective and antioxidant activities.

View Article and Find Full Text PDF
Article Synopsis
  • The study investigates the effects of montelukast (MLK), a cysteinyl leukotriene receptor antagonist, on neuroinflammation and metabolic functions in a rat model of Huntington's disease induced by quinolinic acid (QA).
  • Rat subjects were divided into groups receiving either MLK or a vehicle, monitored through MRI and PET imaging over 14 days and later at 4 months to assess neuroinflammatory responses and metabolic changes.
  • Results showed that while MLK did not significantly reduce QA-induced lesions or inflammation markers, it did attenuate some signs of neuroinflammation and altered metabolic connectivity in the brain regions measured.
View Article and Find Full Text PDF

The pathological accumulation of quinolinic acid (QA) is often associated with neuritis and neuronal cell death in several neurodegenerative diseases, through the overproduction of free radicals. Urolithin B and auraptene have been reported to exert potent antioxidant effects - however, little is known about the protective effects of these compounds against QA-induced neurotoxicity. Therefore, this study aimed to explore the protective effects of urolithin B and auraptene against QA-induced neurotoxicity in the SH-SY5Y neuroblastoma cell line.

View Article and Find Full Text PDF

Increased susceptibility to quinolinic acid-induced seizures and long-term changes in brain oscillations in an animal model of glutaric acidemia type I.

J Neurosci Res

April 2022

Neurophysiology and Neurochemistry of Neuronal Excitability and Synaptic Plasticity Laboratory (NNNESP Lab), Biochemistry Department, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

Glutaric acidemia type I (GA-I) is an inborn error of metabolism of lysine, hydroxylysine, and tryptophan, caused by glutaryl-CoA-dehydrogenase (GCDH) deficiency, characterized by the buildup of toxic organic acids predominantly in the brain. After acute catabolic states, patients usually develop striatal degeneration, but the mechanisms behind this damage are still unknown. Quinolinic acid (QA), a metabolite of the kynurenine pathway, increases especially during infections/inflammatory processes, and could act synergically with organic acids, contributing to the neurological features of GA-I.

View Article and Find Full Text PDF

Effects of excitotoxicity in the hypothalamus in transgenic mouse models of Huntington disease.

Heliyon

August 2021

Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, 22184, Lund, Sweden.

Huntington disease (HD) is a fatal neurodegenerative movement disorder caused by an expanded CAG repeat in the huntingtin gene (HTT). The mutant huntingtin protein is ubiquitously expressed, but only certain brain regions are affected. The hypothalamus has emerged as an important area of pathology with selective loss of neurons expressing the neuropeptides orexin (hypocretin), oxytocin and vasopressin in human postmortem HD tissue.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!