Chlorogenic acid, a polyphenol in coffee, protects neurons against glutamate neurotoxicity
The present study has been designed to explore the molecular mechanism of chlorogenic acid (CGA) in the protective effect against glutamate-induced neuronal cell death. Cortical neurons in primary culture were exposed to 300μM l-glutamic acid or vehicle, with or without 10μM CGA or 10μM MK-801. Afte...
Saved in:
Published in | Life sciences (1973) Vol. 139; pp. 69 - 74 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier Inc
15.10.2015
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | The present study has been designed to explore the molecular mechanism of chlorogenic acid (CGA) in the protective effect against glutamate-induced neuronal cell death.
Cortical neurons in primary culture were exposed to 300μM l-glutamic acid or vehicle, with or without 10μM CGA or 10μM MK-801. After 16h, primary cultures were stained with propidium iodide (PI)/Hoechst or calcein. Double-staining with PI and Hoechst was performed to confirm whether cell death induced by glutamate was apoptotic. In addition, intracellular concentrations of Ca2+ were observed using Ca2+ indicator fura-2.
We investigated the protective effects of CGA on glutamate-induced neuronal cell death using primary cultures of mouse cerebral cortex because the release of glutamate during brain ischemia triggers death of neurons. Glutamate-induced neuronal cell death was inhibited by treatment with CGA. In addition, CGA prevented the increase in intracellular concentrations of Ca2+ caused by the addition of glutamate to cultured neurons. On the other hand, there was little effect of CGA on cell death induced by nitric oxide, which is downstream of the ischemic neuronal cell death. Our results suggested that the polyphenol CGA in coffee protects neurons from glutamate neurotoxicity by regulating Ca2+ entry into neurons.
CGA in coffee may have clinical benefits for neurodegenerative diseases such as ischemic stroke. |
---|---|
ISSN: | 0024-3205 1879-0631 |
DOI: | 10.1016/j.lfs.2015.08.005 |