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Xianfeng Gong,Minwei Wang,Shin-ichi Tashiro,Satoshi Onodera,Takashi Ikejima 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.4
A terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay was used to determine that apoptosis causes HeLa cell death induced by pseudolaric acid B. The c-Jun N-terminal kinase (JNK) inhibitor SP600125 decreased p53 protein expression during exposure to pseudolaric acid B. SP600125 decreased the phosphorylation of p53 during pseudolaric acid B exposure, indicating that JNK mediates phosphorylation of p53 during the response to pseudolaric acid B. SP600125 reversed pseudolaric acid B-induced down-regulation of phosphorylated extracellular signal-regulated pro-tein kinase (ERK), and protein kinase C (PKC) was activated by pseudolaric acid B, whereas stau-rosporine, calphostin C, and H7 partly blocked this effect. These results indicate that p53 is partially regulated by JNK in pseudolaric acid B-induced HeLa cell death and that PKC participates in pseudolaric acid B-induced HeLa cell death.
Gong Xian-Feng,Wang Min-Wei,Tashiro Shin-Ichi,Onodera Satoshi,Ikejima Takashi The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.1
Pseudolaric acid B is a major compound found in the bark of Pseudolarix kaempferi Gordon. In our study, pseudolaric acid B inhibited growth of human melanoma cells, A375-S2 in a time and dose-dependent manner. A375-S2 cells treated with pseudolaric acid B showed typical characteristics of apoptosis including morphologic changes, DNA fragmentation, sub-diploid peak in flow cytometry, cleavage of poly-ADP ribose polymerase (PARP) and degradation of inhibitor of caspase-activated DNase (ICAD). P53 protein expression was upregulated while cells were arrested at the $G_2/M$ phase of the cell cycle. There was a decrease in the expression of anti-apoptotic Bcl-2 and Bcl-xL proteins, whereas pro-apoptotic Bax was increased. The two classical caspase substrates, PARP and ICAD, were both decreased in a time-dependent manner, indicating the activation of downstream caspases.
Xian-Feng Gong,Min-Wei Wang,Shin-Ichi Tashiro,Satoshi Onodera,Takashi Ikejima 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.1
Pseudolaric acid B is a major compound found in the bark of Pseudolarix kaempferi Gordon. In our study, pseudolaric acid B inhibited growth of human melanoma cells, A375-S2 in a timeand dose-dependent manner. A375-S2 cells treated with pseudolaric acid B showed typical characteristics of apoptosis including morphologic changes, DNA fragmentation, sub-diploid peak in flow cytometry, cleavage of poly-ADP ribose polymerase (PARP) and degradation of inhibitor of caspase-activated DNase (ICAD). P53 protein expression was upregulated while cells were arrested at the G2/M phase of the cell cycle. There was a decrease in the expression of anti-apoptotic Bcl-2 and Bcl-xL proteins, whereas pro-apoptotic Bax was increased. The two classical caspase substrates, PARP and ICAD, were both decreased in a time-dependent manner, indicating the activation of downstream caspases.
Timosaponin AIII induces apoptosis and autophagy in human melanoma A375-S2 cells
Ye Wang,Lei Xu,Li-Li Lou,Shao-Jiang Song,Guo-Dong Yao,Meng-Yao Ge,Toshihiko Hayashi,Shin-ichi Tashiro,Satoshi Onodera,Takashi Ikejima 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.1
Timosaponin AIII (AIII), a steroidal saponinisolated from Anemarrhena asphodeloides Bge. Our studyshowed that AIII induced both apoptosis and autophagy,and autophagy inhibited apoptosis in A375S2 cells. Furtherly,this study was carried out to investigate what kindof cytokines plays an important role in this process. Theresults revealed that AIII induced apoptosis through activatingc-Jun N-terminal protein kinase (JNK) or extracellularsignal related kinase (ERK) signaling pathway andgenerating NO. However, JNK or ERK inhibited autophagy,while NO had no effect on autophagy. Therefore,JNK, ERK or NO regulates two programmed death processesin different ways. AIII did not show obvious cytotoxiceffect on human peripheral blood mononuclear cells,which indicated that AIII has less side effects on normalcells, and could be considered as a leading compound fordeveloping novel anticancer drug.