Format

Send to

Choose Destination
Neuromolecular Med. 2016 Sep;18(3):474-82. doi: 10.1007/s12017-016-8410-1. Epub 2016 Jun 4.

Protective Effects of AGE and Its Components on Neuroinflammation and Neurodegeneration.

Qu Z1,2, Mossine VV3, Cui J1,2,4, Sun GY1,2,3, Gu Z5,6,7.

Author information

1
Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, M263 Medical Science Building, One Hospital Drive, Columbia, MO, 65212, USA.
2
Center for Translational Neuroscience, University of Missouri School of Medicine, Columbia, MO, 65212, USA.
3
Department of Biochemistry, University of Missouri School of Medicine, Columbia, MO, 65211, USA.
4
Harry S. Truman Veterans Hospital, Columbia, MO, 65212, USA.
5
Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, M263 Medical Science Building, One Hospital Drive, Columbia, MO, 65212, USA. guze@health.missouri.edu.
6
Center for Translational Neuroscience, University of Missouri School of Medicine, Columbia, MO, 65212, USA. guze@health.missouri.edu.
7
Harry S. Truman Veterans Hospital, Columbia, MO, 65212, USA. guze@health.missouri.edu.

Abstract

Garlic (Allium sativum) is used for culinary and medicinal purposes in diverse cultures worldwide. When fresh garlic is soaked in aqueous ethanol under ambient environment over 4 months or longer, the majority of irritating taste and odor is eliminated and the antioxidant profile in the resulting aged garlic extract (AGE) changes significantly. Recently, AGE and its components have been demonstrated to exert neuroprotective effects in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and cerebral ischemia. Because of its health supporting potential, there is increasing interest in understanding the antioxidant and anti-inflammatory properties and the underlying mechanisms for its protective effects in heath and disease. There is evidence for AGE to exert its action on distinct signaling pathways associated with oxidative stress and neuroinflammation, although the primary molecular mechanisms remain unclear. By utilizing quantitative proteomic approaches, we demonstrated that AGE and two of its major ingredients, S-allyl-L-cysteine and N (α)-(1-deoxy-D-fructos-1-yl)-L-arginine, can attenuate neuroinflammatory responses in microglial cells through modulation of Nrf2-mediated signaling as well as other oxidative stress-related pathways. These experimental data provide information for the molecular targets of AGE and its components to mitigate neurodegeneration and neuroinflammation and show a promising potential of these compounds as dietary supplements for health maintenance.

KEYWORDS:

Aged garlic extract; Botanical compounds; N α-(1-deoxy-D-fructos-1-yl)-L-arginine; Neurodegenerative diseases; Neuroinflammation; S-allyl-L-cysteine

PMID:
27263111
DOI:
10.1007/s12017-016-8410-1
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center