Planta Med 2008; 74 - PA239
DOI: 10.1055/s-0028-1084237

Protective effects of Aralia cordata on oxidative stress-induced brain damage

HS Ju 1, SO Cho 1, KS Song 2, KH Bae 3, YH Seong 1
  • 1Laboratory of Pharmacology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 361–763, South Korea
  • 2College of Agriculture and Life-Sciences, Kyungpook National University, Daegu, 702–701, South Korea
  • 3College of Pharmacy, Chungnam National University, Taejon, 305–764, South Korea

Oxidative stress in the brain has been increasingly associated with the development of numerous human neurological diseases [1]. During ischemia-reperfusion condition there is a heavy production of the free radicals such as superoxide, hydroxyl radicals and hydrogen peroxide (H2O2) [2]. Aralia cordata (Araliaceae) (AC) is a medicinal plant distributed in Korea, China and Japan. AC has been reported to have the inhibitory activity on COX-1 and COX-2 [3]. The present study was perfomed to investigate the protective effect of aerial part of AC against H2O2-induced neuronal cell damage using cultured neuron and middle cerebral artery occlusion (MCAo)–induced ischemia in rats. AC (5–20µg/ml) inhibited 100µM H2O2-induced neuronal cell death. AC also inhibited H2O2-induced reactive oxygen species (ROS) generation and elevation of intracellular calcium ([Ca2+]i). In vivo, AC (50mg/kg, p.o.) prevented cerebral ischemic injury induced 3h MCAo and 24h reperfusion. The ischemic infarct volume and edema were significantly reduced in rats that received AC, with a corresponding improvement in neurological function. Moreover, AC treatment significantly decreased the histological changes including pyknosis, karyorrhexis, karyolysis and microvacuolation in cortex and hippocampus regions observed following ischemia. Oleanolic acid (OA), isolated from AC as an active component, also inhibited H2O2–induced neuronal cell death, elevation of [Ca2+]i and ROS generation in cultured cortical neurons, suggesting that the neuroprotective effect of AC may be attributable to this compound. In conclusion, AC may act as a candidate in the neurodegenerative diseases such as stroke.

References: 1. Wang, J.Y. et al. (2003)J. Neurosci. Res. 72:508–19.

2. Kaundal, R.K. et al. (2006) Life Sci. 79:2293–302.

3. Lee, I.S. et al. (2006) Arch. Pharm. Res. 29:548–55.