Neuronal Nitric Oxide Synthase (nNOS)/NO, An Accelerator of Melanoma Progression, is a Potential Target for Chemoprevention

Frank L Meyskens,Sun Yang,Zheng Yang,Haitao Ji,Thomas L Poulos,Richard B Silverman

doi:10.1016/j.freeradbiomed.2011.10.416

Abstract

Neuronal Nitric Oxide Synthase (nNOS)/NO, An Accelerator of Melanoma Progression, is a Potential Target for Chemoprevention

Highlights

Title Neuronal Nitric Oxide Synthase/nitric oxide (NO), An Accelerator of Melanoma Progression, is a Potential Target for Chemoprevention
Powered by the California Digital Library University of California peptide (Aβ) in the brain, one of the pathological features of AD, is considered to be a central disease-causing and diseasepromoting event in AD. in this study, we show that feeding male APP/PS1 transgenic mice, a well-established mouse model of AD, with a diet containing phenolic antioxidant tertbutylhydroquinone (TBHQ) for 6 weeks increased the concentration of glutathione (GSH), an important antioxidant, and suppressed the expression of NADPH oxidase 2 (Nox2) as well as lipid peroxidation in the brain
We show that TBHQ diet dramatically reduced brain Aβ load, which was associated with inhibition of the expression of plasminogen activator inhibitor-1 (PAI-1), a redox sensitive protease inhibitor which plays a critical role in brain Aβ accumulation in AD

Summary

Introduction

Title Neuronal Nitric Oxide Synthase (nNOS)/NO, An Accelerator of Melanoma Progression, is a Potential Target for Chemoprevention. Our data suggest that TBHQ may have therapeutic potential for AD through increasing brain antioxidant capacity/reducing oxidative stress level, which leads to inhibition of PAI-1 expression and thereby stimulation of Aβ degradation/clearance from the brain.

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Conclusion