Planta Med 2006; 72 - P_180
DOI: 10.1055/s-2006-949980

Protective effects of catechin and epicatechin from Smilax china rhizome on amyloid β protein (25–35)-induced neurotoxicity in cultured neurons

JY Bana 1, KS Songb 1, YH Seonga 2
  • 1College of Veterinary Medicine and Research Institute of Herbal Medicine, Chungbuk National University, Cheongju, Chungbuk 361–763,South Korea
  • 2College of Agriculture and Life-Sciences, Kyungpook National University, Daegu, 702–701, South Korea

We previously reported that Smilax china L. rhizome inhibits amyloid β protein (25–35) (Aβ (25–35))-induced neurotoxicity in cultured rat cortical neurons [1]. Here, we isolated catechin and epicatechin from S. china rhizome and also studied their neuroprotective effects on Aβ (25–35)-induced neurotoxicity in cultured rat cortical neurons. Catechin and epicatechin inhibited 10µM Aβ (25–35)-induced neuronal cell death at a concentration of 10µM, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Catechin and epicatechin inhibited 10µM Aβ (25–35)-induced elevation of cytosolic calcium concentration ([Ca2+]c), which was measured by a fluorescent dye, Fluo-4 AM. Catechin and epicatechin also inhibited glutamate release into medium induced by 10µM Aβ (25–35), which was measured by HPLC, generation of reactive oxygen species (ROS) and activation of caspase-3. These results suggest that catechin and epicatechin prevent Aβ (25–35)-induced neuronal cell damage by interfering with the increase of [Ca2+]c, and then by inhibiting glutamate release, generation of ROS and caspase-3 activity. Furthermore, these effects of catechin and epicatechin may be associated with the neuroprotective effect of S. china rhizome.

Acknowledgements: This work was supported by a grant from BioGreen 21 Program, Rural Development Administration, Republic of Korea.

Reference: 1. Ban, J.Y., Cho, S.O. et al. (2006), J. Ehthnopharmcol. (in press).