Protective effect of Vitis amurensis against amyloid β protein (25–35)-induced neurotoxicity

Amyloid β protein (Aβ) or Aβ peptide fragments have been suggested to play an important role in the pathogenesis of Alzheimer's disease (AD) [1]. Vitis has been reported to have anti-inflammatory and antioxidative effects [2]. In the present study, the protective effect of Vitis amurensis (VA) against Aβ (25–35)-induced neurotoxicity in primary cultured rat cortical neurons and memory impairment in mice was examined. VA, over a concentration range of 1 to 10µg/ml), concentration-dependently prevented the Aβ (25–35) (10µM)-induced neuronal apoptotic death. VA significantly inhibited Aβ (25–35)-induced elevation of the cytosolic Ca²⁺ concentration ([Ca²⁺]_c) and generation of reactive oxygen species (ROS). In addition, viniferin (0.1–3µM), isolated from VA as an active compound, inhibited Aβ (25–35)-induced neuronal cell death, increase of [Ca²⁺]_c and generation of ROS. These results suggest that VA may ameliorate Aβ (25–35)-induced neurotoxicity by interfering with the increase of [Ca²⁺]_c, and generation of ROS [3] and the neuroprotective effect of VA may be attributable to viniferin. In vivo, memory impairment in mice was produced by intracerebroventricular injection of Aβ (25–35) (16 nmol) and was examined by passive avoidance test [4]. Chronic administration of VA (100mg/kg, P.O, 8 days) prevented memory impairment induced by Aβ (25–35). In conclusion, VA may act as a novel and promising therapeutics for the treatment of neurodegenerative diseases including AD.

References: 1. Masters, C.L. et al. (2006)J. Neurochem. 97:1700–25.

2. Rice-Evans, C. A. et al. (1995) Free Radic. Res. 22:375–83.

3. Gunasekar, P.G. et al. (1996)J. Pharmacol. Exp. Ther. 277:150–55.

4. Schwarzberg, H. et al. (1989) Neuropeptides 13:79–81.