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Protective Effects of AGE and Its Components on Neuroinflammation and Neurodegeneration

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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.

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Acknowledgments

This publication was made possible by funding of the 5P01ES016738-02 Missouri Consortium from the National Institute of Environmental Health Science (NIEHS) and the Department of Pathology and Anatomical Sciences research fund at University of Missouri (to ZG), as well as by Grant Number P50AT006273 from the National Center for Complementary and Integrative Health (NCCIH), the Office of Dietary Supplements (ODS), and the National Cancer Institute (NCI). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIEHS, NCCIH, ODS, NCI, or the National Institutes of Health.

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  1. Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, M263 Medical Science Building, One Hospital Drive, Columbia, MO, 65212, USA

    Zhe Qu, Jiankun Cui, Grace Y. Sun & Zezong Gu

  2. Center for Translational Neuroscience, University of Missouri School of Medicine, Columbia, MO, 65212, USA

    Zhe Qu, Jiankun Cui, Grace Y. Sun & Zezong Gu

  3. Department of Biochemistry, University of Missouri School of Medicine, Columbia, MO, 65211, USA

    Valeri V. Mossine & Grace Y. Sun

  4. Harry S. Truman Veterans Hospital, Columbia, MO, 65212, USA

    Jiankun Cui & Zezong Gu

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  1. Zhe Qu
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Correspondence to Zezong Gu.

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Qu, Z., Mossine, V.V., Cui, J. et al. Protective Effects of AGE and Its Components on Neuroinflammation and Neurodegeneration. Neuromol Med 18, 474–482 (2016). https://doi.org/10.1007/s12017-016-8410-1

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