TAILIEUCHUNG - Báo cáo khoa học: Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons

Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca 2+ levels, and nitric oxide-mediated oxidative stress, resulting in DNA damage, poly(ADP-ribose) polymerase (PARP) activation, NAD + deple-tion and cell death. We evaluated the effect of a series of polyphenolic compounds [. epigallocatechin gallate (EPCG), catechin hydrate, curcu-min, apigenin, naringenin and gallotannin] with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons | Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons Nady Braidy1 Ross Grant1 2 Seray Adams1 and Gilles J. Guillemin1 3 1 University of New South Wales Faculty of Medicine Sydney Australia 2 Australasian Research Institute Sydney Adventist Hospital Sydney Australia 3 St Vincent s Centre for Applied MedicalResearch Sydney Australia Keywords Alzheimer s disease excitotoxicity NAD polyphenols quinolinic acid Correspondence G. J. Guillemin Department of Pharmacology Faculty of Medicine University of NSW Sydney 2052 Australia Fax 61 02 9385 1059 Tel 61 02 9385 2548 E-mail Received 5 June 2009 revised 22 October 2009 accepted 9 November 2009 doi Quinolinic acid QUIN excitotoxicity is mediated by elevated intracellular Ca2 levels and nitric oxide-mediated oxidative stress resulting in DNA damage poly ADP-ribose polymerase PARP activation NAD depletion and cell death. We evaluated the effect of a series of polyphenolic compounds . epigallocatechin gallate EPCG catechin hydrate curcu-min apigenin naringenin and gallotannin with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons. We showed that the polyphenols EPCG catechin hydrate and curcumin can attenuate QUIN-induced excitotoxicity to a greater extent than apigenin naringenin and gallotannin. Both EPCG and curcumin were able to attenuate QUIN-induced Ca2 influx and neuronal nitric oxide synthase nNOS activity to a greater extent compared with apigenin naringenin and gallotannin. Although Ca2 influx was not attenuated by catechin hydrate nNOS activity was reduced probably through direct inhibition of the enzyme. All polyphenols reduced the oxidative effects of increased nitric oxide production thereby reducing the formation of 3-nitrotyrosine and poly ADP-ribose polymerase activity and hence preventing NAD depletion and cell death. In addition to the well-known

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