H2O2로 유발된 뇌신경세포 상해에 대한 구진의 보호효과

The protective effects of Moxi-tar on injury induced by H2O2 in C6-glioma

  • 안성훈 (원광대학교 한의과대학 경혈학교실) ;
  • 구성태 (원광대학교 한의과대학 경혈학교실) ;
  • 김선영 (원광대학교 한의과대학 경혈학교실) ;
  • 김경식 (원광대학교 한의과대학 경혈학교실) ;
  • 손인철 (원광대학교 한의과대학 경혈학교실)
  • Ahn, Sung-hun (Dept. of Meridian & Acupoint, College of Oriental Medicine, Wonkwang University) ;
  • Koo, Sung-tae (Dept. of Meridian & Acupoint, College of Oriental Medicine, Wonkwang University) ;
  • Kim, Sun-young (Dept. of Meridian & Acupoint, College of Oriental Medicine, Wonkwang University) ;
  • Kim, Kyung-sik (Dept. of Meridian & Acupoint, College of Oriental Medicine, Wonkwang University) ;
  • Sohn, In-cheul (Dept. of Meridian & Acupoint, College of Oriental Medicine, Wonkwang University)
  • 투고 : 2004.03.19
  • 심사 : 2004.05.15
  • 발행 : 2004.06.20

초록

Objective : This study was produced to examine the effects of moxibustion that had been played important role to traditional oriental medical treatment on disease. Recently, it was reported that moxi-tar which is generated in the process of moxibustion as burning combustibles decreased NO and iNOS generation in C6-glioma and RAW 264.7 cells in our lab. Methods : C6-glioma cells were cultured in RPMI 1640 with FBS 10% in CO2 incubator. To study the protective effects of moxi-tar, we observed cell viability, DPPH activity, SOD activity, catalase activity and cell morphology after injury with $H_2O_2$. Results and Conclusions : Moxi-tar increased cell viability about twice as much as that of being injury by $H_2O_2$(moxi-tar $40{\mu}g/m{\ell}$, $H_2O_2$ $500{\mu}M$). And the results of free radical scavenger activity($80{\mu}g/m{\ell}$ : $78.91{\pm}4.4%$), SOD activity and catalase activity($80{\mu}g/m{\ell}$ : 21.6unit/mg protein) were increased by moxi-tar as dose-dependent manner. So we concluded that the effects of moxibustion which is played important role in Oriental medicine, might be free radical scavenger effects induced by moxi-tar. Conclusion : These results indicate that tBHP induces apoptosis through a lipid peroxidation-dependent mechanism and JS exerts the protective effect against the apoptosis by preventing peroxidation of membrane lipids.

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