본문 바로가기
  • Home

Studies on signal transduction mechanism of alcohol-induced neuronal cell death and protective effect

이도연 1 Sung Su Kim 1 김경용 1 Lee Won Bok 1 김대경 1 김경환 1 Jung, HeeYeon 2 이상형 2

1중앙대학교
2서울대학교

Withdraw

이 논문은 대한체질인류학회 윤리위원회 회의(2020.2.27.) 결과 일부 그림이나 내용이 중복된 점이 확인되어 게재가 철회된 논문임

ABSTRACT

Excessive use of alcohol is a serious problem in our society and induces various, severe alcohol related diseases. The cytotoxicities of ethanol are still largely unknown. We studied the molecular mechanisms of EtOH-induced SK-NSH neuronal cell death and protective effects of baicalein and gramineus against EtOH-induced cytotoxicities.In our results, the cell death by EtOH showed morphologic features of apoptosis like as membrane blebbing, nuclear condensation and fragmentation. Furthermore, pretreated baicalein attenuated EtOH-induced neuronal cell death effectively. EtOH increased expression levels of p53 and both p53 antisense oligonucleotide and Pifithrin protected the cell death against EtOH. Also, EtOH induced mitochondrial event, collapse of mitochondrial membrane potential (∆Ψm) and caspase cascade as a downstream of mitochondria. Interestingly, baicalein decreased expression levels of p53 and inhibited collapse of mitochondrial membrane potential. These results suggest that baicalein reduces mitochondrial dysfunction induced by EtOH through down-regulation of p53 expression levels. Also, baicalein attenuated activation of caspase, which was triggered by mitochondrial malfunction. But gramineus didn’t have any protective effect. These results imply that baicalein significantly protects EtOH-induced neuronal cell death through regulating p53, mitochondrial dysfunction and caspase activation.

Citation status

* References for papers published after 2023 are currently being built.