가미녕신환(加味寧神丸)이 CT105로 유도된 Neuro2A 세포주에서의 항치매 효과(效果)

Study on the Inhibitory Effect of Anti-Alzheimer in CT105-induced Neuro 2A Cell Lines by Gamiyaungshinhwan Water Extract

  • 방재선 (대구한의대학교 한의과대학 심계내과학교실) ;
  • 윤현덕 (대구한의대학교 한의과대학 심계내과학교실) ;
  • 신오철 (대구한의대학교 한의과대학 심계내과학교실) ;
  • 신유정 (대구한의대학교 한의과대학 심계내과학교실) ;
  • 박치상 (대구한의대학교 한의과대학 심계내과학교실)
  • Bang, Jae-Sun (Department of Internal Medicine, College of Oriental medicine, Daegu Haany University) ;
  • Yoon, Hyun-Duk (Department of Internal Medicine, College of Oriental medicine, Daegu Haany University) ;
  • Shin, Oh-Chul (Department of Internal Medicine, College of Oriental medicine, Daegu Haany University) ;
  • Shin, Yoo-Jung (Department of Internal Medicine, College of Oriental medicine, Daegu Haany University) ;
  • Park, Chi-Sang (Department of Internal Medicine, College of Oriental medicine, Daegu Haany University)
  • 발행 : 2006.09.30

초록

The water extract of Gamiyaengshinhwan (GYH), has been used in vitro tests for its beneficial effects on neuronal survival and neuroprotective functions, particularly in connection with CT105-related dementias and Alzheimer's disease(AD). CT105 derived from proteolytic processing of the $\beta$-amyloid precursor protein (APP), including the amyloid-$\beta$ peptide ($A{\beta}$), plays a critical role in the pathogenesis of Alzheimer's dementia. We determined that transfected overexpressing APP695 and $A{\beta}$ CT105 have a profound attenuation in the Increase in CT105 expressing neuro2A cells from GYH. Experimental evidence indicates that GYH protects against neuronal damage from cells, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing CT105-associated neuronal degeneration, we demonstrated that GYH inhibits formation of amyloid-$\beta$ fragment ($A{\beta}$ CT105). which are the characteristic, and possibly causative, features of AD. The decreased CT105 $A{\beta}$ in the presence of GYH was observed in the conditioned medium of this CT105-secreting cell line under in vitro. In the cells, GYH significantly attenuated mitochondrion-initiated apoptosis and decreased the activity of Bax, a key enzyme in the apoptosis cell-signaling cascade. These results suggest that neuronal damage in AD might be due to two factors: a direct CT05 toxicity and the apoptosis initiated by the mitochondria. Multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of CT105 aggregation, underlie the neuroprotective effects of GYH.

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