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Oridonin induces apoptosis of HeLa cells via altering expression of Bcl-2/Bax and activating caspase-3/ICAD pathway

Acta Pharmacologica Sinica 2004年第5期25卷 149-156页

作者： Shin-ichi TASHIRO,satoshi onodera,Takashi IKEJIMA Department of Clinical and Biomedical Sciences Showa College of Pharmaceutical Sciences Tokyo 194-8543 Japan Department of Clinical and Biomedical Sciences Showa College of Pharmaceutical Sciences Tokyo 194-8543 Japan China-Japan Research Institute of Medical and Pharmaceutical Sciences Shenyang Pharmaceutical University Shenyang 110016 China prof

AIM: To study the mechanisms by which oridonin inhibited HeLa cell growth in vitro. METHODS: Viability oforidonin-induced HeLa cells was measured by MTT assay. Apoptotic cells with condensed nuclei were visualizedby phase contrast microscopy. Nucleosomal DNA fragmentation was assayed by agarose gel *** activity was assayed using fluorometric protease assay. ICAD, Bcl-2, and Bax proteins expression weredetected by Western blot analysis. RESULTS: Oridonin induced oligonucleosomal fragmentation of DNA andincreased caspase-3 activity, on the other hand, reduced the expression of inhibitor of caspase-3-activated DNase(ICAD), a caspase-3 substrate, at 12 h in HeLa cells. Oridonin-induced DNA fragmentation, caspase-3 activationand down-regulation of ICAD expression were effectively inhibited by a caspase-3 inhibitor, z-DEVD-fmk (z-Asp-Glu-Val-Asp-fmk). However, pretreatment with an inhibitor of poly (ADP-ribose) polymerase (PARP), 3, 4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone (DPQ), did not suppress oridonin-induced HeLa cell death. Inaddition, oridonin-induced apoptosis was associated with an increase in the expression of the apoptosis inducerBax, and a significant reduction in expression of the apoptosis suppressor Bcl-2 in mitochondria. CONCLUSION:Oridonin induces HeLa cells apoptosis by altering balance of Bcl-2 and Bax protein expression and activation ofcaspase-3/ICAD pathway.

关键词： oridonin HeLa cells apoptosis caspase 3 caspases bcl-2 genes bax genes Western blotting

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Evodiamine induces tumor cell death through different pathways: apoptosis and necrosis

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Acta Pharmacologica Sinica 2004年第1期 85-91页

作者： Shin-ichi TASHIRO,satoshi onodera,Takashi IKEJIMA Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543 Japan Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543 Japan China-Japan Research Institute of Medical and Pharmaceutical Sciences Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543 Japan

AIM: To study the different death pathways in human cervical cancer HeLa and melanoma A375-S2 cells Initiated by evodiamine. METHODS: Viability of evodiamine-induced HeLa and A375-S2 cells was measured by MTT assay. Apoptotic cells with condensed or fragmented nuclei were visualized by Hoechst 33258 staining. Nucleoso mal DNA fragmentation was assayed by agarose gel electrophoresis. Proportion of cell death through apoptotic and necrotic pathways was determined by LDH activity-based cytotoxicity assays. Cell cycle distribution was observed by flow cytometry. RESULTS: Evodiamine induced HeLa and A375-S2 cell death dose- and time-dependently. Caspase-3 and -8 were activated in apoptosis induced by evodiamine 15μmol/L. However, over 24- h

关键词： evodiamine apoptosis necrosis caspases MAP kinase signaling system

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Norcantharidin induces apoptosis in HeLa cells through caspase, MAPK, and mitochondrial pathways

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Acta Pharmacologica Sinica 2004年第11期 118-124页

作者： Shin-ichi TASHIRO,satoshi onodera,Takashi IKEJIMA Department of Pharmacology Department of Pharmacology Department of Clinical and Biomedical Sciences Shenyang Pharmaceutical University Shenyang 110016 China Shenyang Pharmaceutical University Shenyang 110016 China Showa Pharmaceutical University Tokyo 19-8543 Japan

AIM: To investigate the mechanism of norcantharidin (NCTD)-induced HeLa cell apoptosis. METHODS: HeLa cell growth inhibition was measured by MTT method. Apoptosis was detected by Hoechst 33258 staining and agarose gel electrophoresis. Caspase activities were assayed using caspase apoptosis detection kit. Western blot analysis was used to evaluate the level of ICAD, ERK/p-ERK, JNK/p-JNK, and Bcl-XL/Bax expression. RESULTS: Norcantharidin inhibited HeLa cell growth in a time- and dose-dependent manner. HeLa cells treated with norcantharidin showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. Caspase family inhibitor (z-VAD-fmk), caspase-8, -9 inhibitor (z-IETD-fmk, Ac-LEHD-CHO, respectively) and caspase-3 inhibitor (z-DEVD-fmk) partially prevent norcantharidin-induced apoptosis, but initiator caspase-1 inhibitor (Ac-YVAD-fmk) did not. The activities of caspase-3, -8, and -9 were up-regulated after norcantharidin treatment. Furthermore, NCTD-induced activat

关键词： norcantharidin HeLa cells apoptosis caspases Bcl-2 family MAP kinase signaling system

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Diosgenin induces apoptosis in HeLa cells via activation of caspase pathway

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Acta Pharmacologica Sinica 2004年第8期 103-108页

作者： Shin-ichi TASHIRO,satoshi onodera,Takashi IKEJIMA China Department of Clinical and Biomedical Sciences Department of Clinical and Biomedical Sciences China-Japan Research Institute of Medical and Pharmaceutical Sciences Showa Pharmaceutical University Tokyo 194-8543 Japan Showa Pharmaceutical University Tokyo 194-8543 Japan Shenyang Pharmaceutical University

AIM: To investigate the mechanism of diosgenin-induced HeLa cell apoptosis. METHODS: HeLa cell growth was measured by MTT method. Apoptosis was detected by electron microscopy and agarose gel electrophoresis. Ratio of apoptotic cells was measured by APO-BRDU kit. Cell cycle distribution and changes of mitochondrial membrane potential were monitored by flow cytometry. Caspase activities were assayed by caspase apoptosis detection kit. Western blot analysis was used to evaluate the level of mitochondrial Bcl-2 expression. RESULTS: Diosgenin inhibited HeLa cell growth. HeLa cells treated with diosgenin showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. Caspase family inhibitor (z-VAD-fmk), caspase-9 inhibitor (Ac-AAVALPAVLLALLAPLEHD-CHO), and caspase-3 inhibitor (z-DEVD-fmk) partially prevented diosgenin-induced apoptosis, but not caspase-8 inhibitor (z-IETD-fmk) and caspase-10 inhibitor (z-AEVD-fmk). Diosgenin caused reduction of mitochondrial membrane po

关键词： diosgenin apoptosis caspases mitochondria HeLa cells

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Pseudolaric acid B induces apoptosis,senescence,and mitotic arrest in human breast cancer MCF-7

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Acta Pharmacologica Sinica 2007年第12期28卷 1975-1983页

作者： Shin-ichi TASHIRO satoshi onodera Takashi IKEJIMA Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543Japan China-Japan Research Institute of Medical Pharmaceutical Sciences Shenyang Pharmaceutical UniversityShenyang 110016China

Aim:The aim of the present study was to investigate the inhibitory effect ofpseudolaric acid B （PAB） on human breast cancer MCF-7 ***:3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis,morphologicalchanges,acridine orange staining,and agarose gel electrophoresis were appliedto detect *** percentage of apoptotic and necrotic cells was calcu-lated by the lactate dehydrogenase activity-based cytotoxicity assay;senescenceassociated （SA）-β-galactosidase activity was detected to evaluate senescence;flow cytometric analysis of propidium iodide staining was carried out to investi-gate the distribution of cell cycle,and the protein expression was examined byWestern blot ***:During apoptosis,the half maximal inhibitoryconcentration IC50was 3.4 and 1.35 μmol/L at 36 and 48 h after PAB treatment,*** MCF-7 cells exposed to PAB showed typical characteristics ofapoptosis,including the morphological changes and DNA ***-7 cells treated with 4 μmol/L PAB for 36 h underwent apoptosis,but *** apoptosis induced by PAB was independent of the death *** senescent cells became larger and flatter,and the SA-β-galactosi-dase staining was *** induced obvious mitotic arrest and it precededapoptosis and *** expressions of p21 and p53 was upregulated withPAB treatment,and cyclin B 1 was upregulated and transported from the cyto-plasm to nuclei,and sustained stable ***:PAB induced mitoticarrest in the MCF-7 cells and inhibited proliferation through apoptosis *** apoptosis was independent of the death receptor pathway.

关键词： apoptosis senescence mitotic arrest human breast cancer MCF-7 pseudolaric acid B

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Involvement of mitochondria and caspase pathways in N-demethyl-clarithromycin-induced apoptosis in human cervical cancer HeLa cell

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Acta Pharmacologica Sinica 2006年第12期27卷 1622-1629页

作者： Takashi IKEJIMA Shin-ichi TASHIRO satoshi onodera China-Japan Research Institute of Medical Pharmaceutical Sciences Shenyang Pharmaceutical UniversityShenyang 110016China Department of Clinical and Biomedical Sciences Showa Pharmaceutical UniversityTokyo 194-8543Japan

Aim:To study the mechanisms by which N-demethyl-clarithromycin(NDC)induces human cervical cancer HeLa cell apoptosis in ***:The viabilityof N-demethyl-clarithromycin-induced HeLa cells was measured by MTT *** cells with condensed nuclei were visualized by phase *** DNA fragmentation was assayed by agarose *** of mitochondrial transmembrane potential wasanalyzed by a FACScan ***-3,poly-(ADP-ribose)polymerase(PARP),caspase-activated DNase(ICAD),Bcl-2,Bax,p53,and SIRT1 proteinexpression and the release of cytochrome c were detected by Western blot ***:N-demethyl-clarithromycin,an anti-inflammatory substance,inhibitedHeLa cell growth in a dose-and time-dependent manner.N-demethyl-clarithro-mycin induced HeLa cell death through the apoptotic *** pan-caspaseinhibitor(z-VAD-fmk),caspase-3 inhibitor(z-DEVD-fmk)and the caspase-9 inhibi-tor(z-LEHD-fmk)partially enhanced cell viability induced by N-demethyl-clarithromycin,but the caspase-8 inhibitor(z-IETD-fmk)had almost no ***-3 was activated then followed by the degradation of caspase-3 substrates,the inhibitor of ICAD and PARE Simultaneously,mitochondrial transmembranepotential was markedly reduced and the release of cytochrome c in the cytosolwas increased.N-demethyl-clarithromycin upregulated the expression ratio ofmitochondrial Bax/Bcl-2,and significantly increased the expression of the *** also downregulated anti-apoptotic protein SIRT1 ***:N-demethyl-clarithromycin induced apoptosis in HeLa cells via themitochondrial pathway.

关键词： N-demethyl-clarithromycin HeLa cells caspase mitochondria

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P53-mediated cell cycle arrest and apoptosis through a caspase-3-independent,but caspase-9-dependent pathway in oridonin-treated MCF-7 human breast cancer cells

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Acta Pharmacologica Sinica 2007年第7期28卷 1057-1066页

作者： Shin-ichi TASHIRO satoshi onodera Mutsuhiko MINAMI Takashi IKEJIMA Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543Japan Department of ImmunologyYokohama City University School of Medicine Yokohama 235-0004Japan China-Japan Research Institute of Medical Pharmaceutical Sciences Shenyang Pharmaceutical UniversityShenyang 110016China

Aim:To study the caspase-3-independent mechanisms in oridonin-induced MCF-7human breast cancer cell apoptosis in ***:The viability of oridonin-treated MCF-7 cells was measured by MTT （thiazole blue） *** cellswith condensed nuclei were visualized by phase contrast ***-mal DNA fragmentation was assayed by agarose gel *** apoptoticratio was determined by lactate dehydrogenase *** cycle alternation andmitochondrial membrane potential were measured by flow cytometric ***,Bcl-2,caspase-3,caspase-9,heat shock protein （Hsp）90,p53,p-p53,p21,Poly（ADP-ribose） polymerase （PARP）,and the inhibitor of caspase-activated DNase（ICAD） protein expressions were detected by Western blot ***:Oridonin inhibited cell growth in a time-and dose-dependent *** cyclewas altered through the upregulation of p53 and p21 protein ***-caspase inhibitor Z-VAD-fmk and calpain inhibitor Ⅱ both decreased cell *** DNA fragmentation and the downregulation of ΔΨmitweredetected in oridonin-induced MCF-7 cell apoptosis,which was involved in apostmitochondrial caspase-9-dependent *** Bcl-2 and Hsp90expression levels and increased Bax and p21 expression levels were positivelycorrelated with elevated levels of phosphorylated p53 ***,PARP was partially cleaved by calpain rather than by ***:DNAdamage provoked alternations in the mitochondrial and caspase-9 pathways aswell as p53-mediated cell cycle arrest,but was not related to caspase-3 activity inoridonin-induced MCF-7 cells.

关键词： oridonin MCF-7 cells cell cycle arrest apoptosis p53 caspase-9 caspase-3 calpain mitochondrial pathway

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Activation of extracellular signal-regulated kinase during silibinin-protected,isoproterenol-induced apoptosis in rat cardiac myocytes is tyrosine kinase pathway-mediated and protein kinase C-dependent

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Acta Pharmacologica Sinica 2007年第6期28卷 803-810页

作者： Shin-ichi TASHIRO satoshi onodera Fumiaki UCHIUMI Takashi IKEJIMA Department of Clinical and BiomedicalSciences Showa Pharmaceutical UniversityTokyo 194-8543Japan Department of Gene Regulation Faculty of Pharmaceutical SciencesTokyo University of ScienceChiba 278-8510Japan China-Japan Research Institute of Medieal and Pharmaceutical Sciences Shenyang Pharmaceutical UniversityShenyang 110016China

Aim:To investigate the mechanism of silibinin-protected isoproterenol-inducedapoptosis in rat cardiac ***:The viability of rat cardiac myocyteswas measured by MTT *** apoptotic ratio was measured by terminaldeoxynucleotidyl transferase-mediated dUTP nick *** kinase C(PKC) activity assay was carried out according to the instructions of the PepTagnon-radioactive protein kinase C assay *** blot analysis was used toevaluate the level of Ras,Raf-1 and mitogen-activated protein kinase (MAPK)***:The protective effects of silibinin were significantly sup-pressed by inhibitors,including genistein,manumycin A and GW5074 [inhibitorsfor protein tyrosine kinases (PTK),Ras and Raf-1,respectively].The exposure ofrat cardiac myocytes to isoproterenol alone caused decreased PKC activity,whichwas prevented by pretreatment with silibinin ***,the increased expression of Ras and Raf-1 activated by silibinin were blocked bythe PKC inhibitor,*** addition,the extracellularly responsive kinase(ERK) inhibitor,PD98059,suppressed silibinin-protected apoptosis,whereas thep38 MAPK inhibitor,SB203580,protected cardiac myocytes from isoproterenol-induced injury,and the c-Jun N-terminal kinase (JNK) inhibitor,SP600125 had noprotective ***,Western blot analysis showed that the expres-sion of phosphorylated ERK was increased by silibinin,the expression of phos-phorylated p38 MAPK was decreased and total ERK,p38,JNK and phosphory-lated JNK MAPK did not change after treatment with both isoproterenol ***,pretreatment of cardiac myocyte with PKC,Ras and Rafinhibitors significantly blocked ERK ***:Silibinin issuggested to protect isoproterenol-induced rat cardiac myocyte apoptosis byactivating the tyrosine kinase pathway,PKC and MAPK pathways.

关键词： silibinin rat cardiac myocytes tyrosine kinase: protein kinase C mitngen-activated protein kinases

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冬凌草甲素通过诱导人宫颈癌HeLa细胞自噬下调凋亡的机制

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药学学报 2007年第1期42卷 35-39页

作者：崔侨田代真一小野寺敏池岛乔沈阳药科大学中日医药研究所辽宁沈阳110016 昭和药科大学病态科学教研室

研究冬凌草甲素通过诱导人宫颈癌HeLa细胞自噬拮抗凋亡的机制。MTT法测定冬凌草甲素对HeLa细胞的细胞毒作用。通过相差显微镜观察细胞形态学变化,用琼脂糖凝胶电泳检测DNA片段化,用流式细胞仪检测细胞自噬和凋亡水平,用Westernblotting... 详细信息

研究冬凌草甲素通过诱导人宫颈癌HeLa细胞自噬拮抗凋亡的机制。MTT法测定冬凌草甲素对HeLa细胞的细胞毒作用。通过相差显微镜观察细胞形态学变化,用琼脂糖凝胶电泳检测DNA片段化,用流式细胞仪检测细胞自噬和凋亡水平,用Westernblotting检测分析药物对蛋白质表达的影响。冬凌草甲素明显抑制HeLa细胞的增殖,诱导HeLa细胞凋亡,同时诱导HeLa细胞发生自噬。Westernblotting检测结果表明,冬凌草甲素作用24h后,促凋亡蛋白Bax、细胞色素c和控制Bax活力的去乙酰化酶SIRT-1的表达明显改变。冬凌草甲素(64μmol.L-1)诱导的自噬通过影响SIRT-1和线粒体途径蛋白的表达下调凋亡。

关键词：冬凌草甲素 HeLa细胞自噬细胞凋亡

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Mitogen-activated protein kinase-dependent apoptosis in norcan-tharidin-treated A375-S2 cells is proceeded by the activation of protein kinase C

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中华医学杂志(英文版) 2005年第3期000卷 23-28页

作者： AN Wei-wei, WANG Min-wei, Tashiro Shin-ichi, onodera satoshi and Ikejima TakashiChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016, China Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University, Tokyo 19-8543, Japan China-Japan Research Institute of Medical and Pharmaceutical Sciences Shenyang Pharmaceutical University Shenyang 110016 China Department of Pharmacology Shenyang Pharmaceutical University Shenyang 110016 China Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 19-8543 Japan

Background We have reported that norcantharidin (NCTD) induces human melanoma A375-S2 cell apoptosis and that the activation of caspase and the mitochondrial pathway are involved in the apoptotic process. This study aimed at investigating the roles of mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) in A375-S2 cell apoptosis induced by NCTD.

关键词： norcantharidin · A375-S2 cells · mitogen-activated protein kinase · protein kinase C · staurosporine

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