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KMID : 1123920090230020397
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Korean Journal of Oriental Physiology and Pathology
2009 Volume.23 No. 2 p.397 ~ p.404
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Standardization of Quality and Inhibitory Effect of Alzheimer in Oligomer-induced H19-7 Cells by LMK02
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Kang Hyung-Won
Kim Sang-Tae
Son Hyung-Jin
Han Pyeong-Leem
Cho Hyoung-Kwon
Lee Young-Jae
Lyu Yeoung-Su
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Abstract
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For standardization of LMK02 quality, Ginsenoside Rg3 of Red Ginseng and Decursin of Angelica gigas Nakai in the constituents of LMK02 were estimated as indicative components. From LMK02 water extract, has been used in vitro test for its beneficial effects on neuronal survival and neuroprotective functions, particularly in connection with APP-related dementias and Alzheimer’s disease (AD). oligomer derived from proteolytic processing of the -amyloid precursor protein (APP), including the amyloid- peptide (), play a critical role in the pathogenesis of Alzheimer’s dementia. We determined that oligomer amyloid- () have a profound attenuation in the increase in rat hippocampus H19-7 cells from. Experimental evidence indicates that LMK02 protects against neuronal damage from cells, but its cellular and molecular mechanisms remain unknown. Using a hippocampus cell line on oligomer-induced neuronal cytotoxicity, we demonstrated that LMK02 inhibits formation of oligomer, which are the behavior, and possibly causative, feature of AD. In the Red Ginseng, the average amounts of Ginsenoside Rg3 were and , 90 % of its weight were set as a standard value. And, in the Angelica gigas Nakai, the average amounts of Decursin were 2.71 mg/g and 2.44mg/g, 90 % of its weight were also set as a standard value. The attenuated oligomer in the presence of LMK02 was observed in the conditioned medium of this oligomer-induced cells under in vitro. In the cells, LMK02 significantly activated antiapoptosis and decreased the production of ROS. These results suggest that neuronal damage in AD might be due to two factors: a direct oligomer toxicity and multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of oligomer, underlie the neuroprotective effects of LMK02 treatment.
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KEYWORD
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oligomer, H19-7, hippocampus, alzhemiers disease, LMK02, ginsenoside Rg3, decursin
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