Ethanol Extract of Three Plants of Curcuma longae Radix, Phellinus linteus, and Scutellariae Radix Inhibits Amyloid β Protein (25-35)-Induced Neurotoxicity in Cultured Neurons and Memory Impairment in Mice
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The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid β protein (Aβ) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to 10 μM Aβ (25-35) for 36 h induced neuronal apoptotic death. At 1-50㎍/㎖, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS) induced by Aβ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Aβ (25-35) was inhibited by chronic treatment with HS0608 (25, 50 and 100 ㎎/㎏, p.o. for 7 days) as measured by a passive avoidance test. From these results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against Aβ (25-35)-induced neurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer’s disease.
Abstract
The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid β protein (Aβ) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to 10 μM Aβ (25-35) for 36 h induced neuronal apoptotic death. At 1-50㎍/㎖, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS) induced by Aβ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Aβ (25-35) was inhibited by chronic treatment with HS0608 (25, 50 and 100 ㎎/㎏, p.o. for 7 days) as measured by a passive avoidance test. From these results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against Aβ (25-35)-induced neurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer’s disease.
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