The present study investigated an ethanol extract (SSB) of a mixture of three medicinal plants of Vitisamurensis, Aralia cordata, and Glycyrrhizae radix for possible neuroprotective effects on neurotoxicity induced byAmyloid β protein (Aβ) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cor-tical neurons to 15μM Aβ (25-35) for 36h induced neuronal apoptotic death. At 1-30㎍/㎖, SSB inhibited neuronal death,elevation of intracellular calcium concentration ([Ca²+]i), and generation of reactive oxygen species (ROS) induced by Aβ(25-35) in cultured cortical neurons. Memory impairment and increase of acetylcholinesterase activity induced by intra-cerebroventricular injection of mice with 16nmol Aβ (25-35) was inhibited by chronic treatment with SSB (25, 50 and100㎎/㎏, p.o., for 8 days). From these results, it is suggested that antidementia effect of SSB is due to its neuroprotectiveeffect against Aβ (25-35)-induced neurotoxicity and that SSB may have a therapeutic role in preventing the progression ofAlzheimer’s disease.

The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcumalongae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid βprotein (Aβ) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to10µM Aβ (25-35) for 36h induced neuronal apoptotic death. At 1-50㎍/㎖, HS0608 inhibited neuronal death, elevation of intra-cellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS) induced by Aβ (25-35) in primary cul-tures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Aβ (25-35) wasinhibited by chronic treatment with HS0608 (25, 50 and 100㎎/㎏, p.o. for 7 days) as measured by a passive avoidance test. Fromthese results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against Aβ (25-35)-inducedneurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer’s disease.