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.
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Curr Drug Discov Technol
July 2023
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
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 PDFJ Neuroinflammation
February 2023
Nuclear Medicine Department, San Raffaele Scientific Institute (IRCCS), Milan, Italy.
Altern Lab Anim
January 2023
Department of Clinical Biochemistry, Faculty of Medicine, 37552Mashhad University of Medical Sciences, Mashhad, Iran.
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 PDFJ 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 PDFHeliyon
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.
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