AI Article Synopsis
- Oxidative stress contributes to neurodegenerative diseases, and the study evaluates the neuroprotective effects of two caffeoylquinic acid derivatives, 3,5-diCQA and 3,4-diCQA, derived from Dipsacus asper against hydrogen peroxide-induced neuronal damage.
- H2O2 exposure led to decreased cell survival, reduced intracellular glutathione, and increased caspase-3 activity in neuronal SH-SY5Y cells.
- Pretreating cells with 3,5-diCQA helped reduce neuronal death and caspase-3 activation while restoring glutathione levels, suggesting its potential as a therapeutic agent against oxidative stress-related neurodegenerative diseases.
Article Abstract
Oxidative stress plays an important role in the pathological processes of a variety of neurodegenerative diseases. The neuroprotective effects of 3,5-diCQA and 3,4-diCQA, two caffeoylquinic acid derivatives present in Dipsacus asper, on hydrogen peroxide (H2O2)-induced neuronal cell damage were evaluated in this study.SH-SY5Y cells treated with H2O2 exhibited a decrease in survival and intracellular glutathione and also an increase in the caspase-3 activity. However, pretreatment of cells with 3,5-diCQA attenuated the neuronal death and caspase-3 activation induced by H2O2. In addition, 3,5-diCQA restored H2O2-induced depletion of intracellular glutathione. 3,5-diCQA showed significant protective effects although it could not completely suppress H2O2-induced cell injury to control levels. The data suggest that 3,5-diCQA might be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress.
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| http://dx.doi.org/10.1002/ptr.1652 | DOI Listing |
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