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        HL-60 세포의 Apoptosis에 대한 가미항백탕의 효과

        정상필 ( Sang Pil Chung ),김경수 ( Kyeong Su Kim ),송정섭 ( Jung Sup Song ),박성혁 ( Seong Heak Park ),정문재 ( Moon Jae Jung ),이수경 ( Su Kyung Lee ),권영달 ( Young Dal Kwon ),송용선 ( Yung Sun Song ) 한방재활의학과학회 2007 한방재활의학과학회지 Vol.17 No.1

        Objectives: To investigate anti-leukemic effect of Gamihangbak-tang(Jiaweikangbai-tang) using human promyelocytic leukemic HL-60 cells. Methods : Cell viability was determined using MTT assay. Morphological change was observed under a fluorescence microscope through DAPI-Methol staining. DNA fragmentation was analyzed by agarose gel electrophoresis. Caspase activity was measured by using a fluorogenic caspase substrate. Cleavage f caspase-3, PARP and Bid, expression of Bcl-2 and Bax, release of cytochrome C, and activation of MAPKs (ERK, JNK, p38) were determined by Western blot analysis. Results : Gamihangbak-tang(Jiaweikangbai-tang) treated HL-60 cells increased time-dependently DNA fragments and apoptotic bodies. Activities of caspase-3, 8, 9 increased on 30min after Gamihangbak-tang(Jiaweikangbai-tang) treatment and greatly increased after 3h treatment. PARP cleavage also increased 89 kDa PARP fragment on 3hr after Gamihangbak-tang(Jiaweikangbai-tang) treatment. Expression of Bcl-2 and Bax in Gamihangbak-tang (Jiaweikangbai-tang) treated HL-60 cells was not changed, but caspase-8-dependent Bid cleavage was observed. Gamihangbak-tang(Jiaweikangbaitang) also induced cytochrome C release from mitochondria into the cytosol. Activation of ERK, p38, and JNK increased in apoptosis induced by Gamihangbak-tang(Jiaweikangbai-tang) in HL-60 cells, but only ERK activation was concerned in Gamihangbak-tang(Jiaweikangbai-tang)-induced apoptosis. Conclusions : Apoptosis induced by Gamihangbak-tang(Jiaweikangbai-tang) in HL-60 cells induce caspase-3 activation through Bid cleavage by caspase-8, caused cytochrome C release from mitochondria, and ERK activation

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