Journal of Physiology & Pathology in Korean Medicine (동의생리병리학회지)

The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine (대한동의생리학회·한의병리학회)
권호 표지

Machanism of Cisplatin-induced Apoptosis and Bojungbangam-tang-mediated Anti-apoptotic Effect on Cell Proliferation in Rat Mesangial Cells

Cisplatin과 보정방암탕에 의한 백서 사구체 혈관사이세포의 세포사멸 기전 연구

  • Ju, Sung Min (Department of Pathology, College of Korean Medicine, Wonkwang University) ;
  • Kim, Sung Hoon (Cancer Preventive Material Development Research Center, College of Korean Medicine, Kyunghee University) ;
  • Kim, Yeong Mok (Department of Pathology, College of Korean Medicine, Wonkwang University) ;
  • Jeon, Byung Hun (Department of Pathology, College of Korean Medicine, Wonkwang University) ;
  • Kim, Won Sin (Department of Biological Science, College of Natural Sciences, Wonkwang University)
  • 주성민 (원광대학교 한의과대학 병리학교실) ;
  • 김성훈 (경희대학교 한의과대학 암예방소재개발연구센터) ;
  • 김영목 (원광대학교 한의과대학 병리학교실) ;
  • 전병훈 (원광대학교 한의과대학 병리학교실) ;
  • 김원신 (원광대학교 자연과학대학 생명과학부)
  • Received : 2013.02.13
  • Accepted : 2013.02.18
  • Published : 2013.02.25
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Abstract

Cisplatin is a anti-neoplastic agent which is commonly used for the treatment of solid tumor. Cisplatin activates multiple signal transduction pathways involved in the stress-induced apoptosis in a variety of cell types. Previous study reported that cisplatin induces apoptosis through activation of ERK, p38 and JNK in rat mesangial cells, but apoptotic pathway remain known. The present study investigated the apoptotic pathway for cisplatin-indcued apoptosis in rat mesangial cells. cisplatin-induced apoptosis was associated with activation of caspase-3, caspase-8, caspase-9. Caspase-8 inhibition prevented the activation of both caspase-3 and caspase-9. In addition, cisplatin-induced apoptosis increased the expression of Bax, but not the level of Bcl-2. These change of Bax/bcl-2 ratio caused the release of cytochrome c from mitochondria into cytosol. In previous study, the ethanol extract of Bojungbangam-tang (EBJT) inhibited cisplatin-induced apoptosis in rat mesangial cells through inhibition of ERK and JNK activation. However, EBJT did not increase cell proliferation, because it did not prevent cisplatin-induced G2/M phase arrest. These effect of EBJT may be related to p38 activation. Cisplatin-induced G2/M phase arrest are inhibited by treatment with p38 inhibitor and EBJT in rat mesangial cells. Also, p38 inhibition and EBJT treatment on cisplatin-induced G2/M phase arrest are markedly increased the G0/G1 phase and reduced the sub-G1. In conclusion, anti-apoptotic effet of EBJT did not increases cell proliferation, because EBJT did not reduce p38 activation related to cisplatin-induced G2/M phase arrest.

Keywords

References

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