The memory ameliorating effects of INM-176, an ethanolic extract of Angelica gigas, against scopolamine- or Aβ1–42-induced cognitive dysfunction in mice

Autor: In-Ho Jung, Jun Man Jung, Hyung Eun Lee, Se Jin Park, Dae Sik Jang, Chang Hwan Lee, Jong Min Kim, Yong-Baik Cho, Young Woo Lee, Jin Gyu Hong, Jong Hoon Ryu, Dong-Hyun Kim
Rok vydání: 2012
Předmět:
Zdroj: Journal of Ethnopharmacology. 143:611-620
ISSN: 0378-8741
DOI: 10.1016/j.jep.2012.07.019
Popis: Ethnopharmacological relevance Alzheimer’s disease is a neurodegenerative disorder associated with cognitive impairment and cholinergic neuronal death. INM-176 is a standardized ethanolic extract of Angelica gigas Nakai that has been traditionally used in herbal medicine in China, Japan, and Korea to treat anemia or as a sedative. We investigated whether INM-176 exhibits anti-amnesic effects. Materials and methods Memory impairment was induced by scopolamine, a cholinergic muscarinic receptor antagonist, or amyloid β 1–42 (Aβ 1–42 ) protein. Anti-amnesic effects of INM-176 were measured by the passive avoidance and the Morris water maze tasks in mice. We also examined the effect of INM-176 on the acetylcholinesterase activity, as well as Aβ 1–42 protein-induced astrogliosis or cholinergic neuronal loss in the brain. Results Scopolamine-induced cognitive dysfunction was significantly attenuated by a single or sub-chronic administration of INM-176 in the passive avoidance and the Morris water maze tasks. A single or sub-chronic administration of INM-176 also ameliorated memory impairments induced by Aβ 1–42 protein. INM-176 inhibited acetylcholinesterase activity in the hippocampal tissue in vitro and ex vivo . In addition, INM-176 attenuated the Aβ 1–42 protein-induced astrocyte activation in the hippocampus as well as cholinergic neuronal damage in the CA3 region of the hippocampus and the nucleus basalis of Meynert. Conclusion These results suggest that the memory ameliorating effects of INM-176 on scopolamine- or Aβ 1–42 protein-induced memory impairment are mediated, in part, via acetylcholinesterase inhibition and neuroprotective activities.
Databáze: OpenAIRE