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Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review)

  • Authors:
    • Yasuhiro Kosuge
  • View Affiliations / Copyright

    Affiliations: Laboratory of Pharmacology, School of Pharmacy, Nihon University, Funabashi-shi, Chiba 274-8555, Japan
    Copyright: © Kosuge et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1565-1569
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    Published online on: December 27, 2019
       https://doi.org/10.3892/etm.2019.8391
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Abstract

S‑allyl‑L‑cysteine (SAC) is a sulfur‑containing amino acid present in garlic and exhibits a wide range of biological activities such as antioxidant, anti‑inflammatory, and anticancer agent. An earlier study demonstrated that SAC ameliorates oxidative damage in a model of experimental stroke. However, the antioxidant property of SAC does not suffice to explain its beneficial effects in terms of the underlying mechanisms. Endoplasmic reticulum (ER) stress and ER stress‑induced cell death have been shown to be involved in various neurological diseases such as brain ischemia, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and Huntington's disease. We have previously demonstrated that SAC exerts significant protective effects against ER stress‑induced neurotoxicity in cultured rat hippocampal neurons and organotypic hippocampal slice cultures. Recently, we demonstrated that these results are due to the direct suppression of calpain activity via the binding of SAC to this enzyme's Ca2+‑binding domain. We also found that the protective effects of the side‑chain‑modified SAC derivatives, S‑ethyl‑L‑cysteine (SEC) and S‑propyl‑L‑cysteine (SPC), against ER stress‑induced neurotoxicity were more potent than those of SAC in cultured rat hippocampal neurons. In addition, SAC, SEC and SPC have been shown to decrease the production of amyloid‑β peptide in the brains of mice with D‑galactose‑induced aging. These three hydrophilic cysteine‑containing compounds have also been shown to exert neuroprotective effects against dopaminergic neuron injury in a murine model of Parkinson's disease induced by 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP). In this review, we aim to provide a current overview of the protective actions of SAC and the SAC‑related compounds, SEC and SPC, in neurodegenerative disease and discuss the promise of SAC as a prototype for developing novel therapeutic drugs for neurological diseases.
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Copy and paste a formatted citation
Spandidos Publications style
Kosuge Y: Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review). Exp Ther Med 19: 1565-1569, 2020.
APA
Kosuge, Y. (2020). Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review). Experimental and Therapeutic Medicine, 19, 1565-1569. https://doi.org/10.3892/etm.2019.8391
MLA
Kosuge, Y."Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review)". Experimental and Therapeutic Medicine 19.2 (2020): 1565-1569.
Chicago
Kosuge, Y."Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review)". Experimental and Therapeutic Medicine 19, no. 2 (2020): 1565-1569. https://doi.org/10.3892/etm.2019.8391
Copy and paste a formatted citation
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Spandidos Publications style
Kosuge Y: Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review). Exp Ther Med 19: 1565-1569, 2020.
APA
Kosuge, Y. (2020). Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review). Experimental and Therapeutic Medicine, 19, 1565-1569. https://doi.org/10.3892/etm.2019.8391
MLA
Kosuge, Y."Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review)". Experimental and Therapeutic Medicine 19.2 (2020): 1565-1569.
Chicago
Kosuge, Y."Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease (Review)". Experimental and Therapeutic Medicine 19, no. 2 (2020): 1565-1569. https://doi.org/10.3892/etm.2019.8391
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