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Protective Effects of Curcumin on Amyloid-β-Induced Neuronal Oxidative Damage

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Abstract

To investigate the protective effects of curcumin against amyloid-β (Aβ)-induced neuronal damage. Primary rat cortical neurons were cultured with different treatments of Aβ and curcumin. Neuronal morphologies, viability and damage were assessed. Neuronal oxidative stress was assessed, including extracellular hydrogen peroxide and intracellular reactive oxygen species. The abilities of curcumin to scavenge free radicals and to inhibit Aβ aggregation and β-sheeted formation are further assessed and discussed. Curcumin preserves cell viability, which is decreased by Aβ. The results of changed morphology, released Lactate dehydrogenases and cell viability assays indicate that curcumin protects Aβ-induced neuronal damage. Curcumin depresses Aβ-induced up-regulation of neuronal oxidative stress. The treatment sequence impacts the protective effect of curcumin on Aβ-induced neuronal damage. Curcumin shows a more protective effect on neuronal oxidative damage when curcumin was added into cultured neurons not later than Aβ, especially prior to Aβ. The abilities of curcumin to scavenge free radicals and to inhibit the formation of β-sheeted aggregation are both beneficial to depress Aβ-induced oxidative damage. Curcumin prevents neurons from Aβ-induced oxidative damage, implying the therapeutic usage for the treatment of Alzheimer’s disease patients.

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Acknowledgments

This research was supported by Project 31071512 Supported by National Natural Science Foundation of China, Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality (PHR(IHLB)) [PHR20090514], and Scientific Research Common Program of Beijing Municipal Commission of Education (KM201011417002).

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Correspondence to Zhao-Feng Jiang.

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Huang, HC., Chang, P., Dai, XL. et al. Protective Effects of Curcumin on Amyloid-β-Induced Neuronal Oxidative Damage. Neurochem Res 37, 1584–1597 (2012). https://doi.org/10.1007/s11064-012-0754-9

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  • DOI: https://doi.org/10.1007/s11064-012-0754-9

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