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[PMID]:29238189
[Au] Autor:Zhang CY; Sun XY; Ouyang JM; Gui BS
[Ad] Endereço:Institute of Biomineralization and Lithiasis Research, Jinan University, Guangzhou.
[Ti] Título:Diethyl citrate and sodium citrate reduce the cytotoxic effects of nanosized hydroxyapatite crystals on mouse vascular smooth muscle cells.
[So] Source:Int J Nanomedicine;12:8511-8525, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Objective: This study aimed to investigate the damage mechanism of nanosized hydroxyapatite (nano-HAp) on mouse aortic smooth muscle cells (MOVASs) and the injury-inhibiting effects of diethyl citrate (Et Cit) and sodium citrate (Na Cit) to develop new drugs that can simultaneously induce anticoagulation and inhibit vascular calcification. Methods: The change in cell viability was evaluated using a cell proliferation assay kit, and the amount of lactate dehydrogenase (LDH) released was measured using an LDH kit. Intracellular reactive oxygen species (ROS) and mitochondrial damage were detected by DCFH-DA staining and JC-1 staining. Cell apoptosis and necrosis were detected by Annexin V staining. Intracellular calcium concentration and lysosomal integrity were measured using Fluo-4/AM and acridine orange, respectively. Results: Nano-HAp decreased cell viability and damaged the cell membrane, resulting in the release of a large amount of LDH. Nano-HAp entered the cells and damaged the mitochondria, and then induced cell apoptosis by producing a large amount of ROS. In addition, nano-HAp increased the intracellular Ca concentration, leading to lysosomal rupture and cell necrosis. On addition of the anticoagulant Et Cit or Na Cit, cell viability and mitochondrial membrane potential increased, whereas the amount of LDH released, ROS, and apoptosis rate decreased. Et Cit and Na Cit could also chelate with Ca to inhibit the intracellular Ca elevations induced by nano-HAp, prevent lysosomal rupture, and reduce cell necrosis. High concentrations of Et Cit and Na Cit exhibited strong inhibitory effects. The inhibitory capacity of Na Cit was stronger than that of Et Cit at similar concentrations. Conclusion: Both Et Cit and Na Cit significantly reduced the cytotoxicity of nano-HAp on MOVASs and inhibited the apoptosis and necrosis induced by nano-HAp crystals. The chelating function of citrate resulted in both anticoagulation and binding to HAp. Et Cit and Na Cit may play a role as anticoagulants in reducing injury to the vascular wall caused by nano-HAp.
[Mh] Termos MeSH primário: Citratos/farmacologia
Durapatita/efeitos adversos
Músculo Liso Vascular/citologia
Nanopartículas/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/farmacologia
Apoptose/efeitos dos fármacos
Calcinose/prevenção & controle
Cálcio/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Durapatita/química
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Nanopartículas/química
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Citrates); 0 (Reactive Oxygen Species); 0 (diethyl citrate); 1Q73Q2JULR (sodium citrate); 91D9GV0Z28 (Durapatite); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S145386


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[PMID]:29441966
[Au] Autor:Zhao H; Meng W; Li Y; Liu W; Fu B; Yang Y; Zhang Q; Chen G
[Ti] Título:The protective effects of CHIR99021 against oxidative injury in LO2 cells.
[So] Source:Pharmazie;71(11):629-635, 2016 11 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Hepatic ischemia-reperfusion injury is one of the most important factors for the prognosis of liver transplantation and hepatic surgery. It was reported that glycogen synthase kinase-3 (GSK-3) regulated injury response during ischemia-reperfusion. In this study, we investigated the protective effects of the GSK-3 inhibitor CHIR99021 against hepatic ischemia-reperfusion injury. A H2O2-induced oxidative injury model using LO2 cells was established. LO2 cells were divided into four groups, including blank control group, CHIR99021 control group treated with CHIR99021 alone, H2O2-injury group treated with H2O2 and protection group treated with H2O2 plus CHIR99021. Cell viability, cell apoptosis or necrosis was determined. Meanwhile, mitochondrial membrane potential, lipid peroxidation, cellular ROS levels, SOD activity, and serum contents of ALS and AST were measured. Protein and mRNA expressions were also detected. The results showed that a cell oxidative injury model was established by treating LO2 cells with 200 µmol/L H2O2 for 6 h. Cells exposed to H2O2 resulted in a significant decrease of cell viability and increase of cell apoptosis, which was accompanied by increasing ROS levels, disruption of mitochondrial membrane potential, excessive lipid peroxidation, reduction of SOD activity, and increased levels of ALT and AST. Treatment with CHIR99021 significantly protected LO2 cells against H2O2-induce oxidative injury by inhibiting the changes of above oxidative injury related indicators. Moreover, CHIR99021 treatment significantly reversed H2O2-induced decrease in p-GSK-3ßSer9 , Bcl-2, Bcl-xl, survivin and ß-catenin expression, whereas it significantly attenuated H2O2-induced increase in caspase-3, cleaved caspase-3 and p-JNK protein expression. In conclusion, CHIR99021 protected LO2 cells against H2O2-induced oxidative injury through reducing GSK-3ß activity and apoptosis, with underlying mechanisms involved in stabilizing mitochondrial membrane potential, attenuating cellular ROS generation, suppressing mitochondria-mediated apoptotic pathway, and activation of GSK-3ß/ß-catenin signaling pathway.
[Mh] Termos MeSH primário: Citoproteção/efeitos dos fármacos
Hepatócitos/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Piridinas/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Apoptose/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Doença Hepática Induzida por Substâncias e Drogas/enzimologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Quinase 3 da Glicogênio Sintase/biossíntese
Quinase 3 da Glicogênio Sintase/genética
Seres Humanos
Peróxido de Hidrogênio/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Necrose
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Chir 99021); 0 (Pyridines); 0 (Pyrimidines); BBX060AN9V (Hydrogen Peroxide); EC 2.7.11.26 (Glycogen Synthase Kinase 3)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6714


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[PMID]:29442032
[Au] Autor:Jiang JF; Zhai J; Liu ZR; Chao L; Zhao YF; Wu YJ; Cui MX
[Ti] Título:Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line.
[So] Source:Pharmazie;71(8):455-459, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ampelopsin is a well-known flavonoid which has variety of biological and pharmacological actions including anticancer effects and induction of apoptosis on the several cancer cell lines. The present study aimed to evaluate the role of ampelopsin sodium (Amp-Na) in the mitochondrial-mediated apoptosis of human lung adenocarcionma SPC-A-1 cells. The analysis of cell proliferation and ultrastructure were performed. Furthermore, to clarify its action mechanism by determining the mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) level and total ATPase activity. The results showed that Amp-Na markedly inhibited the SPC-A-1 cell proliferation and caused ultrastructural apoptosis feature in SPC-A-1 cells in a dose-dependent manner. Amp-Na led to a rapid and sustained Ca2+ elevation and Δψm reduction, and induced the mitochondrial NO production and decreased the total ATPase activity in SPC-A-1 cells. The results enhance the potential of Amp-Na as a therapeutic drug for treating lung cancer, and provide new information for mechanism of Amp-Na which induces mitochondrial-mediated apoptosis in tumor cells.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma/ultraestrutura
Adenosina Trifosfatases/metabolismo
Cálcio/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Relação Dose-Resposta a Droga
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/ultraestrutura
Potencial da Membrana Mitocondrial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Flavonoids); 27200-12-0 (ampelopsin); EC 3.6.1.- (Adenosine Triphosphatases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6571


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[PMID]:28454554
[Au] Autor:Mittal S; Sharma PK; Tiwari R; Rayavarapu RG; Shankar J; Chauhan LKS; Pandey AK
[Ad] Endereço:Academy of Scientific and Innovative Research (AcSIR), CSIR-IITR Campus, Lucknow, India.
[Ti] Título:Impaired lysosomal activity mediated autophagic flux disruption by graphite carbon nanofibers induce apoptosis in human lung epithelial cells through oxidative stress and energetic impairment.
[So] Source:Part Fibre Toxicol;14(1):15, 2017 Apr 28.
[Is] ISSN:1743-8977
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Graphite carbon nanofibers (GCNF) have emerged as a potential alternative of carbon nanotubes (CNT) for various biomedical applications due to their superior physico-chemical properties. Therefore in-depth understanding of the GCNF induced toxic effects and underlying mechanisms in biological systems is of great interest. Currently, autophagy activation by nanomaterials is recognized as an emerging toxicity mechanism. However, the association of GCNF induced toxicity with this form of cell death is largely unknown. In this study, we have assessed the possible mechanism; especially the role of autophagy, underlying the GCNF induced toxicity. METHODS: Human lung adenocarcinoma (A549) cells were exposed to a range of GCNF concentrations and various cellular parameters were analyzed (up to 48 h). Transmission electron microscopy, immunofluorescent staining, western blot and quantitative real time PCR were performed to detect apoptosis, autophagy induction, lysosomal destabilization and cytoskeleton disruption in GCNF exposed cells. DCFDA assay was used to evaluate the reactive oxygen species (ROS) production. Experiments with N-acetyl-L-cysteine (NAC), 3-methyladenine (3-MA) and LC3 siRNA was carried out to confirm the involvement of oxidative stress and autophagy in GCNF induced cell death. Comet assay and micronucleus (MN) assay was performed to assess the genotoxicity potential. RESULTS: In the present study, GCNF was found to induce nanotoxicity in human lung cells through autophagosomes accumulation followed by apoptosis via intracellular ROS generation. Mechanistically, impaired lysosomal function and cytoskeleton disruption mediated autophagic flux blockade was found to be the major cause of accumulation rather than autophagy induction which further activates apoptosis. The whole process was in line with the increased ROS level and their pharmacological inhibition leads to mitigation of GCNF induced cell death. Moreover the inhibition of autophagy attenuates apoptosis indicating the role of autophagy as cell death process. GCNF was also found to induce genomic instability. CONCLUSION: Our present study demonstrates that GCNF perturbs various interrelated signaling pathway and unveils the potential nanotoxicity mechanism of GCNF through targeting ROS-autophagy-apoptosis axis. The current study is significant to evaluate the safety and risk assessment of fibrous carbon nanomaterials prior to their potential use and suggests caution on their utilization for biomedical research.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Grafite/toxicidade
Lisossomos/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Nanofibras/toxicidade
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células A549
Sobrevivência Celular/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Seres Humanos
Pulmão/efeitos dos fármacos
Tamanho da Partícula
Espécies Reativas de Oxigênio/metabolismo
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 7782-42-5 (Graphite)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1186/s12989-017-0194-4


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[PMID]:29421517
[Au] Autor:Xue J; Li R; Zhao X; Ma C; Lv X; Liu L; Liu P
[Ad] Endereço:Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, 107 West Wenhua Road, Jinan, 250012, Shandong Province, People's Republic of China. Electronic address: 201620468@mail.sdu.edu.cn.
[Ti] Título:Morusin induces paraptosis-like cell death through mitochondrial calcium overload and dysfunction in epithelial ovarian cancer.
[So] Source:Chem Biol Interact;283:59-74, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Epithelial ovarian cancer (EOC) is the leading cause of death among all gynecological cancers. Morusin, a prenylated flavonoid extracted from the root bark of Morus australis, has been reported to exhibit anti-tumor activity against various human cancers except EOC. In the present study, we explored the potential anti-cancer activity of morusin against EOC in vitro and in vivo and possible underlying mechanisms for the first time. We first found that morusin effectively inhibited EOC cell proliferation and survival in vitro and suppressed tumor growth in vivo. Then we observed that treatment of EOC cells with morusin resulted in paraptosis-like cell death, a novel mode of non-apoptotic programmed cell death that is characterized by extensive cytoplasmic vacuolation due to dilation of the endoplasmic reticulum (ER) and mitochondria and lack of apoptotic hallmarks. In addition, we discovered that morusin induced obvious increase in mitochondrial Ca levels, accumulation of ER stress markers, generation of reactive oxygen species (ROS), and loss of mitochondrial membrane potential (Δψm) in EOC cells. Furthermore, pretreatment with 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS), a chemical inhibitor of voltage-dependent anion channel (VDAC) on the outer mitochondrial membrane, effectively inhibited mitochondrial Ca influx, cytoplasmic vacuolation and cell death induced by morusin in EOC cells. Moreover, DIDS pretreatment also suppressed morusin-induced accumulation of ER stress markers, ROS production and depletion of Δψm. Consistently, tumor xenograft assays showed that co-treatment with DIDS partially reversed the inhibitory effects of morusin on tumor growth in vivo and inhibited the increased levels of ER stress markers induced by morusin in tumor tissues. Collectively, our results suggest that VDAC-mediated Ca influx into mitochondria and subsequent mitochondrial Ca overload contribute to mitochondrial swelling and dysfunction, leading to morusin-induced paraptosis-like cell death in EOC. This study may provide alternative therapeutic strategies for EOC exhibiting resistance to apoptosis.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Cálcio/metabolismo
Flavonoides/farmacologia
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Autofagia/efeitos dos fármacos
Linhagem Celular Tumoral
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Feminino
Flavonoides/química
Flavonoides/uso terapêutico
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Mitocôndrias/metabolismo
Morus/química
Morus/metabolismo
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Epiteliais e Glandulares/patologia
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Flavonoids); 0 (Reactive Oxygen Species); 62596-29-6 (morusin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


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[PMID]:29223571
[Au] Autor:Perdigão GMC; Lopes MS; Marques LB; Prazeres PHDM; Gomes KS; de Oliveira RB; Pinto MCX; de Souza-Fagundes EM
[Ad] Endereço:Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:Novel nitroaromatic compound activates autophagy and apoptosis pathways in HL60 cells.
[So] Source:Chem Biol Interact;283:107-115, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:N-(2-butanoyloxyethyl)-4-(chloromethyl)-3-nitrobenzamide (NBCN) is a nitroaromatic bioreducible compound with cytotoxic effects in cancer cell lines. The aim of this work was to investigate the molecular mechanisms involved in cell death promoted by NBCN in HL60 cells. We observed that NBCN treatment increased intracellular ROS and reduced mitochondria membrane potential (ΔΨm). NBCN treatment also induced morphological changes, phosphatidylserine exposure, cell cycle arrest in G2/M-phase, DNA condensation and fragmentation, but it did not show cytotoxic effects on normal human peripheral blood mononuclear cells (PBMCs). NBCN-induced caspase 3- and 9-dependent DNA fragmentation, which was blocked by pretreatment with the broad-spectrum caspase inhibitor, z-VAD-fmk. Flow cytometry analysis demonstrated that NBCN also increased of the number of autophagic vesicles in HL60 cells, which was not observed when cells were pre-treated with bafilomycin A1. Taken together, these results indicate that NBCN triggered the mitochondrial apoptotic pathway and led to the onset of autophagic cell death, which contributed to its cytotoxic effects.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Benzamidinas/toxicidade
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Benzamidinas/química
Inibidores de Caspase/farmacologia
Caspases/metabolismo
Células Cultivadas
Fragmentação do DNA/efeitos dos fármacos
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Células HL-60
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/metabolismo
Pontos de Checagem da Fase M do Ciclo Celular/efeitos dos fármacos
Macrolídeos/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (Benzamidines); 0 (Caspase Inhibitors); 0 (Macrolides); 0 (Reactive Oxygen Species); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 3459-99-2 (3-nitrobenzamidine); 88899-55-2 (bafilomycin A1); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


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[PMID]:28460467
[Au] Autor:Chen P; Zhang JY; Sha BB; Ma YE; Hu T; Ma YC; Sun H; Shi JX; Dong ZM; Li P
[Ad] Endereço:Cancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
[Ti] Título:Luteolin inhibits cell proliferation and induces cell apoptosis via down-regulation of mitochondrial membrane potential in esophageal carcinoma cells EC1 and KYSE450.
[So] Source:Oncotarget;8(16):27471-27480, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In current study, we investigated the anti-tumor effect of luteolin in human ESCC cell lines in vitro and in vivo and tried to explore the potential mechanisms. Results from flow cytometry showed that luteolin could induce apoptosis and caspase-3 activation and induce cell cycle arrest at G2/M phase in a dose- and time-dependent manner in EC1 and KYSE450 cells. JC-1 test results showed that membrane potential of mitochondria after luteolin treatment was down-regulated and this was an indicator for intrinsic apoptosis. Western Blot results showed the expression of cell cycle regulatory protein p21 and p53 increased and three apoptosis related proteins that participate in mitochondrial apoptotic pathway, namely, Bim, CYT-c and cPARP, also increased in luteolin treated cells compared with control groups. We further confirmed that luteolin could significantly inhibit the growth of ESCC tumors in xenograft mouse models and no evidence of systemic toxicity was observed. Our results suggest that luteolin can induce cell apoptosis and cell cycle arrest in G2/M phase through mitochondrial pathway in EC1 and KYSE450 cell lines and proper utilization of luteolin might be a practical approach in ESCC chemotherapy.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Luteolina/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proteína 11 Semelhante a Bcl-2/genética
Proteína 11 Semelhante a Bcl-2/metabolismo
Caspase 3/metabolismo
Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Modelos Animais de Doenças
Neoplasias Esofágicas
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Poli(ADP-Ribose) Polimerases/genética
Poli(ADP-Ribose) Polimerases/metabolismo
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bcl-2-Like Protein 11); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Tumor Suppressor Protein p53); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 3.4.22.- (Caspase 3); KUX1ZNC9J2 (Luteolin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15832


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[PMID]:29335212
[Au] Autor:Gupta N; Qayum A; Raina A; Shankar R; Gairola S; Singh S; Sangwan PL
[Ad] Endereço:Bioorganic Chemistry Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
[Ti] Título:Synthesis and biological evaluation of novel bavachinin analogs as anticancer agents.
[So] Source:Eur J Med Chem;145:511-523, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A library of 28 analogs of bavachinin including aliphatic and aromatic ethers, epoxide, chalcone, oxime, semicarbazide, oxime ether and triazole derivatives have been synthesized and evaluated for cytotoxicity against four different human cancer cell lines. Bio-evaluation studies exhibited better cytotoxic profile for many analogs compare to bavachinin. Best results were observed for a 1,2,3-triazole analog (17i) with IC values 7.72, 16.08, 7.13 and 11.67 µM against lung (A549), prostate (PC-3), colon (HCT-116) and breast (MCF-7) cancer cell lines respectively. This analog showed three and four fold improvement in cytotoxicity against HCT-116 and A549 cell lines than parent molecule (1). Structure activity relationship (SAR) study for all synthesized analogs was carried out. Further, mechanistic study of the lead molecule (17i) revealed that it inhibits colony formation and in vitro migration of human colon cancer cells (HCT-116). Also, it induced the morphological changes and mediated the apoptotic cell death of HCT-116 cells with perturbance in mitochondrial membrane potential (MMP) and PARP cleavage.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Flavonoides/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Flavonoides/síntese química
Flavonoides/química
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Estrutura Molecular
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Flavonoids); 19879-30-2 (bavachinin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  9 / 10082 MEDLINE  
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[PMID]:29331753
[Au] Autor:Tang B; Wan D; Wang YJ; Yi QY; Guo BH; Liu YJ
[Ad] Endereço:School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, 510006, PR China.
[Ti] Título:An iridium (III) complex as potent anticancer agent induces apoptosis and autophagy in B16 cells through inhibition of the AKT/mTOR pathway.
[So] Source:Eur J Med Chem;145:302-314, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A new ligand THPDP (THPDP = 11-(6,7,8,9-tetrahydrophenazin-2-yl)dipyrido[3,2-a:2',3'-c]phenazine) and its iridium(III) complex [Ir(ppy) (THPDP)]PF (Ir-1) was synthesized and characterized by elemental analysis, IR, ESI-MS, H NMR and C NMR. The cytotoxicity in vitro of the complex against cancer cells B16, A549, Eca-109, SGC-7901, BEL-7402 and normal NIH 3T3 cell lines was evaluated using MTT method. The IC values of the complex toward B16, A549 and Eca-109 cells are 1.0 ±â€¯0.02, 1.4 ±â€¯0.03 and 1.6 ±â€¯0.06 µM, respectively. The apoptosis was investigated with AO/EB and DAPI staining methods. The complex shows strong ability to inhibit the cell growth in B16, A549 and Eca-109 cells. Ir-1 can induce apoptosis, increase the intracellular ROS level, and cause a decrease in the mitochondrial membrane potential. The intracellular Ca level and the release of cytochrome c were studied under a fluorescent microscope. The cell invasion and autophagy were also performed, and the cell cycle arrest was assayed by flow cytometry. The expression of Bcl-2 family proteins, PI3K, AKT, mTOR, P-mTOR was investigated by western blot. The results show that the complex induces apoptosis through ROS-mediated mitochondria dysfunction and inhibition of AKT/mTOR pathways. These findings are helpful for design and synthesis of iridium(III) complexes as potent anticancer drugs.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Complexos de Coordenação/farmacologia
Irídio/farmacologia
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/química
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Complexos de Coordenação/síntese química
Complexos de Coordenação/química
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Irídio/química
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Estrutura Molecular
Células NIH 3T3
Proteínas Proto-Oncogênicas c-akt/metabolismo
Relação Estrutura-Atividade
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Coordination Complexes); 44448S9773 (Iridium); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


  10 / 10082 MEDLINE  
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[PMID]:29289889
[Au] Autor:Li Y; Gu Z; Zhang C; Li S; Zhang L; Zhou G; Wang S; Zhang J
[Ad] Endereço:Key Laboratory of Chemical Biology of Hebei Province, Key Laboratory of Medicinal Chemistry and Molecular Diagnosis, Ministry of Education, College of Chemistry & Environmental Science, Hebei University, Baoding 071002, China.
[Ti] Título:Synthesis, characterization and ROS-mediated antitumor effects of palladium(II) complexes of curcuminoids.
[So] Source:Eur J Med Chem;144:662-671, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Based on the synthesis of curcumin and its derivatives from aromatic aldehydes, a novel series of palladium(II) complexes with curcumin (or its derivatives) and 2,2'-bipyridine have been synthesized through a directed self-assembly approach that involves spontaneous deprotonation of the curcuminoid ligands in H O/acetone solution. These complexes have been characterized by H ( C) NMR, HRMS and elemental analysis. Crystal structure of 3h has been determined by X-ray diffraction analysis. Their cytotoxicity was tested by MTT. The preliminary results showed that complexes 3d, 3f, 3h have significant inhibition on proliferation of three carcinoma cells such as MCF-7, HeLa and A549 cells, which were more active than cisplatin. Further mechanistic studies indicated that the tested complex 3h arrested the cell cycle in the S phase and can disrupted mitochondrial membrane potential and induced tumor cell apoptosis through reactive oxygen species (ROS)-dependent pathway.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Curcumina/farmacologia
Compostos Organometálicos/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Curcumina/análogos & derivados
Curcumina/química
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Estrutura Molecular
Compostos Organometálicos/síntese química
Compostos Organometálicos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Organometallic Compounds); 0 (Reactive Oxygen Species); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE



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