본문 바로가기
  • Home

Influence of Yeoldahanso-tang on the Hypoxic Damage of Cultured Cerebral Neurons from mouse and SK-N-MC cells

  • Journal of Sasang Constitutional Medicine
  • Abbr : J Sasang Constitut Med
  • 2003, 15(1), pp.72-89
  • Publisher : The Society Of Sasang Constitutional Medicine
  • Research Area : Medicine and Pharmacy > Korean Medicine
  • Received : June 30, 2003
  • Accepted : June 30, 2003
  • Published : June 15, 2003

Soo-jung Park 1 Kim Hyoung-soon 2 Young Chun Bae 3 Lee Sang min 4 Kim Kyung yo 5 Kyoung Sook Won 6 Shim Gyue hearn 7

1원광대학교전주한방병원 사상체질과
2원광대학교 대학원 한의학과
3원광대학교 한의과대학 사상체질과
4원광대학교
5원광대학교 한의과대학 사상체질의학교실
6계명대학교
7상지대학교

ABSTRACT

To elucidate the neuroprotective effect of Yeoldahanso-tang(YHT) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT(SODIUM3,3'-{I-[(PHENYLAMINO) CARBONYL]-3,4-TETRAZOLIUM}- BIS (4-METHOXY-6-NITRO) BENZENE SULFONIC ACID HYDRATE), NR(Neutral red), MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and SRB(Sulforhodamin B) asssay. The activity of catalase and SOD(Superoxide dismutase) was measured by spectrophometry, and TNF−α(Tumor cell necrosis fector−α) and PKC(Protein kinase C) activity was measured after exposure to hypoxia and treatment of YHTWE. Also the neuroprotective effect of YHTWE was researched for the elucidatioion of neuroprotective mechanism. The results were as follows; 1. Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO2 for 2∼26 minutes in these cultures and YHTWE inhibited the decrease of cell viability. 2. H2O2 treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 μM for 6 hours, but YHTWE inhibited the decrease of cell viability. 3. Hypoxia decreased catalase and SOD activity, and also TNF−α and PKC activity in these cultured cerebral neurons, but YHTWE inhibited the decrease of the catalase and SOD activity in these cultures. 4. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c forom mitochondria. YHTWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxicity on cultured mouse cerebral neurons, and the YHTWE has the neuroprotective effect in blocking the neurotoxicity induced by hypoxia in cultured mouse cerebral neurons.

Citation status

* References for papers published after 2022 are currently being built.