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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2018.1
- 수록면
- 159 - 166 (8page)
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The Amyloid b peptide (Ab) is a main component of senile plaques in Alzheimer's disease. Currently, NADPH oxidase (NOX) and mitochondria are considered as primary sources of ROS induced by Ab. However, the contribution of NOX and mitochondria to Ab-induced ROS generation has not been well defined. To delineate the relative involvement of NOX and mitochondria in Ab-induced ROS generation and neuronal death in mouse cortical cultures, we examined the effect of NOX inhibitors, apocynin and AEBSF, and the mitochondria-targeted antioxidants (MTAs), mitotempol and mitoquinone, on Ab-induced ROS generation and neuronal deaths. Cell death was assessed by measuring lactate dehydrogenase efflux in bathing media at 24 and 48 hrs after exposure to Ab1-42. Ab1-42 induced dose- and time-dependent neuronal deaths in cortical cultures. Treatment with 20 mM Ab1-42 markedly and continuously increased not only the DHE fluorescence (intracellular ROS signal), but also the DHR123 fluorescence (mitochondrial ROS signal) up to 8 hrs. Treatment with apocynin or AEBSF selectively suppressed the increase in DHE fluorescence, while treatment with mitotempol selectively suppressed the increase in DHR123 fluorescence. Each treatment with apocynin, AEBSF, mitotempol or mitoquinone significantly attenuated the Ab1-42-induced neuronal deaths. However, any combined treatment with apocynin/AEBSF and mitotempol/mitoquinone failed to show additive effects. These findings indicate that 20 mM Ab1-42 induces oxidative neuronal death via inducing mitochondrial ROS as well as NOX activation in mixed cortical cultures, but combined suppression of intracellular and mitochondrial ROS generation fail to show any additive neuroprotective effects against Ab neurotoxicity.
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참고문헌 (27)
참고문헌 신청
Querfurth HW / 2010 / Alzheimer's disease / N Engl J Med 362:329~344
Butterfield DA / 1997 / beta-amyloid-associated free radical oxidative stress and neurotoxicity: implications for Alzheimer's disease / Chem Res Toxicol 10:495~506
Butterfield DA / 2013 / Amyloid ${\beta}$ -peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression / Antioxid Redox Signal 19:823~835
Sorce S / 2017 / NADPH oxidases as drug targets and biomarkers in neurodegenerative diseases: what is the evidence? / Free Radic Biol Med 112:387~396
Cifuentes-Pagano ME / 2015 / Nox inhibitors & therapies: rational design of peptidic and small molecule inhibitors / Curr Pharm Des 21:6023~6035
Butterfield DA / 1997 / beta-amyloid-associated free radical oxidative stress and neurotoxicity: implications for Alzheimer's disease / Chem Res Toxicol 10:495~506
Butterfield DA / 2013 / Amyloid
Sorce S / 2017 / NADPH oxidases as drug targets and biomarkers in neurodegenerative diseases: what is the evidence? / Free Radic Biol Med 112:387~396
Cifuentes-Pagano ME / 2015 / Nox inhibitors & therapies: rational design of peptidic and small molecule inhibitors / Curr Pharm Des 21:6023~6035
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