Neuroprotective effects of Z-ajoene, an organosulfur compound derived from oil-macerated garlic, in the gerbil hippocampal CA1 region after transient forebrain ischemia

  • Food Chem Toxicol. 2014 Oct;72:1-7. doi: 10.1016/j.fct.2014.06.023.
Dae Young Yoo  1 ,  Woosuk Kim  1 ,  Sung Min Nam  1 ,  Miyoung Yoo  2 ,  Sanghee Lee  2 ,  Yeo Sung Yoon  1 ,  Moo-Ho Won  3 ,  In Koo Hwang  4 ,  Jung Hoon Choi  5
Affiliations
  • 1. Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul 151-742, South Korea.
  • 2. Food Analysis Center, Korea Food Research Institute, Sungnam 463-746, South Korea.
  • 3. Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.
  • 4. Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul 151-742, South Korea. Electronic address: [email protected].
  • 5. Department of Anatomy, College of Veterinary Medicine, Kangwon National University, Chuncheon 200-701, South Korea. Electronic address: [email protected].
PMID: 24997311 DOI: 10.1016/j.fct.2014.06.023
Abstract

The neuroprotective effects of two isomers (Z- and E-) of ajoene, a major compound in oil-macerated garlic products, against ischemic damage were investigated in the gerbil hippocampus. Vehicle (corn oil), Z- or E-ajoenes (25 mg/kg) was orally administered 30 min prior to the induction of transient forebrain ischemia by occlusion of the common carotid arteries for 5 min. One day after ischemia/reperfusion (I/R), I/R-induced hyperactivity significantly reduced in the E- and Z-ajoene-treated groups, compared to that in the vehicle-treated group 5 days after I/R, the number of cresyl violet-positive neurons in the E- and Z-ajoene-treated groups increased, compared to that in the vehicle-treated group. Reactive gliosis in the CA1 region of E- and Z-ajoene-treated groups reduced, compared to that in the vehicle-treated group. These neuroprotective effects were more prominent in Animals treated with Z-ajoene, than in those treated with E-ajoene. In addition, Z-ajoene significantly decreased lipid peroxidation, as indicated by 4-hydroxy-2-nonenal levels in hippocampal homogenates, compared to that observed in the vehicle-treated group at a range of time points after I/R. These results suggested that Z-ajoene protected against I/R-induced delayed neuronal death and gliosis by reducing lipid peroxidation in the gerbil hippocampal CA1 region.

Keywords
Ajoene; Lipid peroxidation; Neuroprotection; Reactive gliosis; Spontaneous motor activity; Transient forebrain ischemia.
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