Journal
JOURNAL OF ETHNOPHARMACOLOGY
Volume 128, Issue 1, Pages 206-212Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2010.01.014
Keywords
Oriental medicine; Alzheimer disease; A beta; beta-amyloid plaque; LMK02-Jangwonhwan; Panax ginseng CA Meyer; Angelica gigas Nakai
Categories
Funding
- Ministry of Health and Welfare, Republic of Korea [B070030]
- Korea Health Promotion Institute [B070030] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Ethnopharmacological relevance: Jangwonhwan, a boiled extract of 12 medicinal plants/mushroom including Korean red ginseng (Panax ginseng C.A. Meyer), has been prescribed for patients with cognitive dysfunction and are believed to induce brain activity enhancement, provide light sedation, and facilitate sound sleep. Aim of the study: The present study was carried out to investigate whether Jangwonhwan has a beneficial effect on the brain of Alzheimer disease. Materials and methods: The transgenic mice of Alzheimer disease, Tg-APPswe/PS1dE9, were fed a modified recipe of Jangwonhwan consisting of a boiled extract of 7 herbs/mushroom (called LMK02-Jangwonhwan) at 400 mg/kg/day of dose for 3 months from 4.5 months of age. Immunohistological and ELISA analyses were used to assess the A beta accumulation and plaque deposition in the brain. Other in vitro and in vivo works were performed to understand the underlying mechanism. Results: LMK02-Jangwonhwan notably reduced A beta(1-42) and A beta(1-40) levels, concomitantly with a reduction of plaque deposition, in the brain of Tg-APPswe/PS1dE9 mice. LMK02-Jangwonhwan partially suppressed oxidative stress accumulation, and prevented the down-regulation of phospho-CREB and calbindin typically seen in the hippocampus of AD-like brains. in vitro study with SH-SY5Y neuroblastoma cells showed that LMK02-Jangwonhwan inhibited oxidative stress and A beta-induced neurotoxicity. Conclusion: The present study suggests that LMK02-Jangwonhwan confers a therapeutic potential to ameliorate AD-like pathology in the brain of Tg-APPswe/PS1dE9 mice. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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