Standardization of Quality and Inhibitory Effect of Alzheimer in $A{\beta}$ Oligomer-induced H19-7 Cells by LMK02

LMK02의 품질규격화와 $A{\beta}$ 올리고머에 의해 유도된 희주해마 H19-7세포주에 미치는 항치매효과

  • 강형원 (원광대학교 한의과대학 한방신경정신과교실) ;
  • 김상태 (이화여자대학교 자연대학 나노과학부 뇌신경 분자연구실) ;
  • 손형진 (이화여자대학교 자연대학 나노과학부 뇌신경 분자연구실) ;
  • 한평림 (이화여자대학교 생명.약학부 뇌신경연구실) ;
  • 조형권 (한풍제약(유)) ;
  • 이영재 (한풍제약(유)) ;
  • 류영수 (원광대학교 한의과대학 한방신경정신과교실)
  • Published : 2009.04.25

Abstract

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). $A{\beta}$ oligomer derived from proteolytic processing of the ${\beta}$-amyloid precursor protein (APP), including the amyloid-${\beta}$ peptide ($A{\beta}$), play a critical role in the pathogenesis of Alzheimer's dementia. We determined that oligomer amyloid-${\beta}$ ($A{\beta}$) 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 $A{\beta}$ oligomer-induced neuronal cytotoxicity, we demonstrated that LMK02 inhibits formation of $A{\beta}$ oligomer, which are the behavior, and possibly causative, feature of AD. In the Red Ginseng, the average amounts of Ginsenoside Rg3 were $47.04{\mu}g/g$ and $42.3{\mu}g/g$, 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 $A{\beta}$ oligomer in the presence of LMK02 was observed in the conditioned medium of this $A{\beta}$ 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 $A{\beta}$ oligomer toxicity and multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of $A{\beta}$ oligomer, underlie the neuroprotective effects of LMK02 treatment.

Keywords

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