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Pesquisa : D12.644.360.075.718.400 [Categoria DeCS]
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[PMID]:29198702
[Au] Autor:Wu D; Liang M; Dang H; Fang F; Xu F; Liu C
[Ad] Endereço:Department of Pediatric Intensive Care Unit, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongq
[Ti] Título:Hydrogen protects against hyperoxia-induced apoptosis in type II alveolar epithelial cells via activation of PI3K/Akt/Foxo3a signaling pathway.
[So] Source:Biochem Biophys Res Commun;495(2):1620-1627, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress is regarded as a key regulator in the pathogenesis of prolonged hyperoxia-induced lung injury, which causes injury to alveolar epithelial cells and eventually leads to development of bronchopulmonary dysplasia (BPD). Many studies have shown that hydrogen has a protective effect in a variety of cells. However, the mechanisms by which hydrogen rescues cells from damage due to oxidative stress in BPD remains to be fully elucidated. This study sought to evaluate the effects of hydrogen on hyperoxia-induced lung injury and to investigate the underlying mechanism. Primary type II alveolar epithelial cells (AECIIs) were divided into four groups: control (21% oxygen), hyperoxia (95% oxygen), hyperoxia + hydrogen, and hyperoxia + hydrogen + LY294002 (a PI3K/Akt inhibitor). Proliferation and apoptosis of AECIIs were assessed using MTS assay and flow cytometry (FCM), respectively. Gene and protein expression were detected by quantitative polymerase chain reaction (q-PCR) and western blot analysis. Stimulation with hyperoxia decreased the expression of P-Akt, P- FoxO3a, cyclinD1 and Bcl-2. Hyperoxic conditions increased levels of Bim, Bax, and Foxo3a, which induced proliferation restriction and apoptosis of AECIIs. These effects of hyperoxia were reversed with hydrogen pretreatment. Furthermore, the protective effects of hydrogen were abrogated by PI3K/Akt inhibitor LY294002. The results indicate that hydrogen protects AECIIs from hyperoxia-induced apoptosis by inhibiting apoptosis factors and promoting the expression of anti-apoptosis factors. These effects were associated with activation of the PI3K/Akt/FoxO3a pathway.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/efeitos dos fármacos
Células Epiteliais Alveolares/metabolismo
Hidrogênio/farmacologia
Hiperóxia/tratamento farmacológico
Hiperóxia/metabolismo
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/tratamento farmacológico
Lesão Pulmonar Aguda/metabolismo
Lesão Pulmonar Aguda/patologia
Células Epiteliais Alveolares/patologia
Animais
Apoptose/efeitos dos fármacos
Proteína 11 Semelhante a Bcl-2/genética
Células Cultivadas
Ciclina D1/genética
Feminino
Proteína Forkhead Box O3/genética
Proteína Forkhead Box O3/metabolismo
Expressão Gênica/efeitos dos fármacos
Genes bcl-2/efeitos dos fármacos
Hidrogênio/metabolismo
Hiperóxia/patologia
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/metabolismo
Gravidez
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Bcl-2-Like Protein 11); 0 (Bcl2l11 protein, rat); 0 (Ccnd1 protein, rat); 0 (Forkhead Box Protein O3); 0 (Foxo3a protein, rat); 0 (RNA, Messenger); 0 (bcl-2-Associated X Protein); 136601-57-5 (Cyclin D1); 7YNJ3PO35Z (Hydrogen); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  2 / 13817 MEDLINE  
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[PMID]:28456769
[Au] Autor:Al Dera H
[Ad] Endereço:Department of Basic Medical Sciences, College of Medicine at King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Kingdom of Saudi Arabia. derah@ksau-hs.edu.sa.
[Ti] Título:Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta.
[So] Source:J Physiol Pharmacol;68(1):47-56, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study was carried out to investigate the expression pattern and role of osteopontin (OPN) in late global ischemia-reperfusion (I/R) injury with or without resveratrol (RES) pre-treatment. Young male rats were divided into 3 groups (n = 12) of I) sham, II) I/R model group and III) I/R + RES. Vehicle and RES (20 mg/kg) were administered to designed groups intraperitoneally 30 days prior global I/R injury (2-VO) induction and continued for 7 days, later. Then, percentages of infarct areas, mRNA levels of OPN, inducible nitric oxide synthase (iNOS) and other biochemical parameter related to endogenous antioxidants activities and inflammation were measured in the cerebral cortices of all groups. Significant elevations in the levels of malondialdehyde (MDA), the inflammatory mediator interleukin 1ß (IL-1ß), chemokines (KC and MIP-2) and adhesive molecules (ICAM-1) as well as parallel reductions in enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and chloramphenicol acetyltransferase (CAT) were observed in the cerebral homogenates of rats with late I/R injury. Associated with these changes, mRNA levels of OPN were significantly downregulated and those of iNOS and Bax were upregulated. All these changes were reversed by in 2-VO I/R induced rats pre-administered RES. These findings suggest that inhibition of sustained inflammatory response driven by IL-1ß, decreased activities of endogenous antioxidants and downregulation of OPN induced upregulation of iNOS play important roles in the pathogenesis of neurodegeneration during late cerebral I/R injury, effects that can be modulated by RES which might explain its neuroprotection effect during late global ischemia.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/tratamento farmacológico
Catalase/metabolismo
Córtex Cerebral/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocinas/metabolismo
Glutationa Peroxidase/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/metabolismo
Masculino
Fármacos Neuroprotetores/uso terapêutico
Óxido Nítrico Sintase Tipo II/genética
Osteopontina/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
Traumatismo por Reperfusão/tratamento farmacológico
Estilbenos/uso terapêutico
Superóxido Dismutase/metabolismo
Regulação para Cima
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (Cxcl2 protein, rat); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Neuroprotective Agents); 0 (Spp1 protein, rat); 0 (Stilbenes); 0 (bcl-2-Associated X Protein); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 147037-79-4 (keratinocyte-derived chemokines); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.15.1.1 (Superoxide Dismutase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  3 / 13817 MEDLINE  
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[PMID]:27771353
[Au] Autor:Peng W
[Ad] Endereço:Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong City, Sichuan 637000, P. R. China; Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Sderot Churchill, Jerusalem, 91240, Israel. Electronic address: pengwei39@hotmail.com.
[Ti] Título:G-CSF treatment promotes apoptosis of autoreactive T cells to restrict the inflammatory cascade and accelerate recovery in experimental allergic encephalomyelitis.
[So] Source:Exp Neurol;289:73-84, 2017 03.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G-CSF is a hematopoietic growth factor that regulates the proliferation, differentiation and survival of myeloid lineage cells, which has protective effects in autoimmune neuroinflammatory diseases such as EAE. Here we use EAE model treated by G-CSF to address the hypothesis that G-CSF inhibits the proliferative response of splenic T cells via the enhancement of apoptosis, and this priming effect of G-CSF depends on the cell cycle. Our results show that G-CSF administration reduced EAE frequency and severity of attacks. The inflammatory cells and demyelination areas were decreased in the CNS of G-CSF-treated mice. G-CSF treatment altered cytokine profiles in vivo to inhibit the productions of IFN-γ, IL-1ß, IL-2, TNF-α, IL-17 and NO, while the secretions of IL-4 and IL-10 were increased. Splenic T cells from G-CSF-treated mice showed significantly lower proliferative response to specific antigen MOG stimulation. G-CSF enhanced the percentage of a CD4 CD25 T cell subset in spleen T cells. Moreover, G-CSF promoted the G0/G1 to S phase transition of MOG autoreactive T cells inducing apoptosis and elevating Bax gene expression of apoptosis marker. These findings indicate that G-CSF treatment induces the apoptosis of MOG autoreactive T cells, which decreases the production of pro-inflammatory cytokines and NO, suppresses the proliferation of autoreactive T cells and elevates a CD4 CD25 T cell subset to inhibit inflammatory infiltration and demyelination within CNS of EAE. The conclusions of G-CSF treatment in EAE mice suggest that G-CSF is clinically applicable and may be considered for future use in therapeutic measures for multiple sclerosis treatment.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Linfócitos T CD4-Positivos/efeitos dos fármacos
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/fisiopatologia
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Recuperação de Função Fisiológica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anexina A5/metabolismo
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Feminino
Adjuvante de Freund/toxicidade
Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Glicoproteína Mielina-Oligodendrócito/toxicidade
Óxido Nítrico/metabolismo
Fragmentos de Peptídeos/toxicidade
Toxina Pertussis/toxicidade
Baço/patologia
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Cytokines); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (bcl-2-Associated X Protein); 0 (myelin oligodendrocyte glycoprotein (35-55)); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 31C4KY9ESH (Nitric Oxide); 9007-81-2 (Freund's Adjuvant); EC 2.4.2.31 (Pertussis Toxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  4 / 13817 MEDLINE  
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[PMID]:29338036
[Au] Autor:Chen WT; Lin GB; Lin SH; Lu CH; Hsieh CH; Ma BL; Chao CY
[Ad] Endereço:Department of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
[Ti] Título:Static magnetic field enhances the anticancer efficacy of capsaicin on HepG2 cells via capsaicin receptor TRPV1.
[So] Source:PLoS One;13(1):e0191078, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Static magnetic field (SMF) has shown some possibilities for cancer therapies. In particular, the combinational effect between SMF and anti-cancer drugs has drawn scientists' attentions in recent years. However, the underlying mechanism for the drug-specific synergistic effect is far from being understood. Besides, the drugs used are all conventional chemotherapy drugs, which may cause unpleasant side effects. In this study, our results demonstrate for the first time that SMF could enhance the anti-cancer effect of natural compound, capsaicin, on HepG2 cancer cells through the mitochondria-dependent apoptosis pathway. We found that the synergistic effect could be due to that SMF increased the binding efficiency of capsaicin for the TRPV1 channel. These findings may provide a support to develop an application of SMF for cancer therapy. The present study offers the first trial in combining SMF with natural compound on anti-cancer treatment, which provides additional insight into the interaction between SMF and anti-cancer drugs and opens the door for the development of new strategies in fighting cancer with minimum cytotoxicity and side effects.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Capsaicina/farmacologia
Magnetismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Cálcio/metabolismo
Proliferação Celular/efeitos dos fármacos
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Microscopia de Fluorescência
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (bcl-2-Associated X Protein); S07O44R1ZM (Capsaicin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191078


  5 / 13817 MEDLINE  
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[PMID]:29232945
[Au] Autor:Su L; Yang JF; Fu X; Dong L; Zhou DY; Sun LM; Gong Z
[Ad] Endereço:School of Food Science and Technology, Dalian Polytechnic University, National Engineering Research Center of Seafood , Number 1 Qinggongyuan, Ganjingzi District, Dalian 116034, P. R. China.
[Ti] Título:Ultraviolet-Ray-Induced Sea Cucumber (Stichopus japonicus) Melting Is Mediated by the Caspase-Dependent Mitochondrial Apoptotic Pathway.
[So] Source:J Agric Food Chem;66(1):45-52, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sea cucumber body-wall melting occurs under certain circumstances. We have shown that apoptosis but not autolysis plays a critical role in the initial stage. However, it is still unclear how apoptosis is triggered in this process. In this study, we examined the levels of reactive oxygen species (ROS), the levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax) proteins, the depolarization of mitochondrial transmembrane potentials, and cytochrome c (Cyt c) release during sea cucumber melting induced by ultraviolet (UV) exposure. We also investigated the contribution of caspase in this process by injecting a pan-caspase inhibitor. Our data showed that UV exposure stimulates ROS production, dysfunction of mitochondria, and the release of Cyt c in sea cucumber coelomic fluid cells and body walls. We found a decrease of Bcl-2 and increase of Bax in the mitochondria after UV exposure. We also demonstrated that these changes are associated with elevated caspase-9 and -3 activity. Finally, our data showed that the inhibition of caspases-9 and -3 using an inhibitor suppresses UV-induced sea cucumber melting. These results suggest that apoptosis during sea cucumber melting is mediated by mitochondrial dysfunction and follows the activation of the caspase-signaling pathway. This study presents a novel insight into the mechanism of sea cucumber melting.
[Mh] Termos MeSH primário: Caspases/metabolismo
Pepinos-do-Mar/fisiologia
Pepinos-do-Mar/efeitos da radiação
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Animais
Apoptose/efeitos da radiação
Inibidores de Caspase/farmacologia
Citocromos c/metabolismo
Potencial da Membrana Mitocondrial/efeitos da radiação
Mitocôndrias/metabolismo
Transporte Proteico/efeitos da radiação
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Pepinos-do-Mar/efeitos dos fármacos
Raios Ultravioleta
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (Caspase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (bcl-2-Associated X Protein); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 9007-43-6 (Cytochromes c); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03888


  6 / 13817 MEDLINE  
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[PMID]:29291406
[Au] Autor:Mañas A; Chen W; Nelson A; Yao Q; Xiang J
[Ad] Endereço:Department of Biology, Illinois Institute of Technology, Chicago, IL 60616, USA.
[Ti] Título:BaxΔ2 sensitizes colorectal cancer cells to proteasome inhibitor-induced cell death.
[So] Source:Biochem Biophys Res Commun;496(1):18-24, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proteasome inhibitors, such as bortezomib and carfilzomib, are FDA approved for the treatment of hemopoietic cancers, but recent studies have shown their great potential for treatment of solid tumors. BaxΔ2, a unique proapoptotic Bax isoform, promotes non-mitochondrial cell death and sensitizes cancer cells to chemotherapy. However, endogenous BaxΔ2 proteins are unstable and susceptible to proteasomal degradation. Here, we screened a panel of proteasome inhibitors in colorectal cancer cells with different Bax statuses. We found that all proteasome inhibitors tested were able to block BaxΔ2 degradation without affecting the level of Baxα or Bcl-2 proteins. Among the inhibitors tested, only bortezomib and carfilzomib were able to induce differential cell death corresponding to the distinct Bax statuses. BaxΔ2-positive cells had a significantly higher level of cell death at low nanomolar concentrations than Baxα-positive or Bax-negative cells. Furthermore, bortezomib-induced cell death in BaxΔ2-positive cells was predominantly dependent on the caspase 8/3 pathway, consistent with our previous studies. These results imply that BaxΔ2 can selectively sensitize cancer cells to proteasome inhibitors, enhancing their potential to treat colon cancer and other solid tumors.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/metabolismo
Inibidores de Proteassoma/administração & dosagem
Proteína X Associada a bcl-2/metabolismo
[Mh] Termos MeSH secundário: Neoplasias Colorretais/patologia
Relação Dose-Resposta a Droga
Células HCT116
Seres Humanos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Proteasome Inhibitors); 0 (bcl-2-Associated X Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180102
[St] Status:MEDLINE


  7 / 13817 MEDLINE  
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[PMID]:27770267
[Au] Autor:Nayak VL; Nagesh N; Ravikumar A; Bagul C; Vishnuvardhan MVPS; Srinivasulu V; Kamal A
[Ad] Endereço:Medicinal Chemistry and Pharmacology, CSIR-Indian Institute of Chemical Technology, Hyderabad, 500007, India.
[Ti] Título:2-aryl benzimidazole conjugate induced apoptosis in human breast cancer MCF-7 cells through caspase independent pathway.
[So] Source:Apoptosis;22(1):118-134, 2017 Jan.
[Is] ISSN:1573-675X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Apoptosis is a representative form of programmed cell death, which has been assumed to be critical for cancer prevention. Thus, any agent that can induce apoptosis may be useful for cancer treatment and apoptosis induction is arguably the most potent defense against cancer promotion. In our previous studies, 2-aryl benzimidazole conjugates were synthesized and evaluated for their antiproliferative activity and one of the new molecule (2f) was considered as a potential lead. This lead molecule showed significant antiproliferative activity against human breast cancer cell line, MCF-7. The results of the present study revealed that this compound arrested the cell cycle at G2/M phase. Topoisomerase II inhibition assay and Western blot analysis suggested that this compound effectively inhibits topoisomerase II activity which leads to apoptotic cell death. Apoptosis induction in MCF-7 cells was further confirmed by loss of mitochondrial membrane potential (∆Ψm), release of cytochrome c from mitochondria, an increase in the level of apoptosis inducing factor (AIF), generation of reactive oxygen species (ROS), up regulation of proapoptotic protein Bax and down regulation of anti apoptotic protein Bcl-2. Apoptosis assay using Annexin V-FITC assay also suggested that this compound induced cell death by apoptosis. However, compound 2f induced apoptosis could not be reversed by Z-VAD-FMK (a pan-caspase inhibitor) demonstrated that the 2f induced apoptosis was caspase independent. Further, 2f treatment did not activate caspase-7 and caspase-9 activity, suggesting that this compound induced apoptosis in breast cancer cells via a caspase independent pathway. Most importantly, this compound was less toxic towards non-tumorigenic breast epithelial cells, MCF-10A. Furthermore, docking studies also support the potentiality of this molecule to bind to the DNA topoisomerase II.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Benzimidazóis/administração & dosagem
Neoplasias da Mama/tratamento farmacológico
DNA Topoisomerases Tipo II/química
[Mh] Termos MeSH secundário: Fator de Indução de Apoptose/genética
Benzimidazóis/química
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Inibidores de Caspase/administração & dosagem
Inibidores de Caspase/química
Caspases/genética
Proliferação Celular/efeitos dos fármacos
DNA Topoisomerases Tipo II/genética
Feminino
Seres Humanos
Células MCF-7
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/genética
Simulação de Acoplamento Molecular
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIFM1 protein, human); 0 (Apoptosis Inducing Factor); 0 (BAX protein, human); 0 (Benzimidazoles); 0 (Caspase Inhibitors); 0 (Reactive Oxygen Species); 0 (bcl-2-Associated X Protein); E24GX49LD8 (benzimidazole); EC 3.4.22.- (Caspases); EC 5.99.1.3 (DNA Topoisomerases, Type II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s10495-016-1290-x


  8 / 13817 MEDLINE  
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[PMID]:29225136
[Au] Autor:Vakamullu S; Arepalli SK; Velatooru LR; J VR; P KK; B N
[Ad] Endereço:Toxicology Unit, Biology Division, CSIR-Indian Institute of Chemical Technology, Hyderabad, 500 607, India; MNR Foundation for Research and Innovation, MNR Medical College, Sangareddy, Telangana, 502294, India.
[Ti] Título:In vitro apoptotic mechanism of a novel synthetic Quinazolinyl derivative: Induces caspase-dependent intrinsic pathway on THP-1, leukemia cell line.
[So] Source:Chem Biol Interact;280:117-127, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Several quinazoline derivatives have been found to possess a broad spectrum of biological activities. Previously our research group has synthesized and studied the anti-proliferative effects of N-Decyl-N-(2-Methyl-4-Quinazolinyl) Amine (DMQA). The current study evaluated the cytotoxic and apoptotic properties of DMQA in THP-1 cells. The cytotoxic potential of DMQA was assessed using MTT assay on a panel of cancer cell lines which include HeLa, Mia PaCa-2, A 375, B16-F10, A 549,A 431, U937, THP-1, HL-60 and peripheral blood mononuclear cells (PBMC's). Preliminary data revealed that the highest cytotoxic activity was against THP-1 leukemia cell line (IC 0.66 µg/ml). The apoptotic properties of DMQA on THP-1 cells were characterized by change in nuclear morphology, DNA fragmentation, reduction of pro-caspases-3, 9, Bax/Bcl-2 levels, cleavage of poly (ADP-ribose) polymerase and cytosolic release of cytochrome c. Further investigation revealed a sub-G1 peak, phosphatidyl serine exposure and loss of mitochondrial membrane potential (MMP) in THP-1 cells. The role of caspases was crucial and was demonstrated by the inhibitors Z-VAD-FMK and Z-DEVD-FMK. Moreover DMQA was markedly less effective in inhibiting the growth of normal cells (PBMC's, IC 62.17 µg/ml). Based on the results we suggest that DMQA induced apoptosis via intrinsic pathway and could be a promising anticancer agent.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Caspases/metabolismo
Quinazolinas/farmacologia
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Caspases/química
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Fragmentação do DNA/efeitos dos fármacos
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Células HL-60
Células HeLa
Seres Humanos
Leucemia/metabolismo
Leucemia/patologia
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Poli(ADP-Ribose) Polimerases/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Quinazolinas/química
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (Antineoplastic Agents); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Quinazolines); 0 (bcl-2-Associated X Protein); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


  9 / 13817 MEDLINE  
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[PMID]:29188738
[Au] Autor:Hu JB; Song GL; Liu D; Li SJ; Wu JH; Kang XQ; Qi J; Jin FY; Wang XJ; Xu XL; Ying XY; Yu L; You J; Du YZ
[Ad] Endereço:a Institute of Pharmaceutics, College of Pharmaceutical Sciences , Zhejiang University , Hangzhou , China.
[Ti] Título:Sialic acid-modified solid lipid nanoparticles as vascular endothelium-targeting carriers for ischemia-reperfusion-induced acute renal injury.
[So] Source:Drug Deliv;24(1):1856-1867, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In an attempt to improve therapeutic efficacy of dexamethasone (DXM)-loaded solid lipid nanoparticles (NPs) for renal ischemia-reperfusion injury (IRI)-induced acute renal injury (AKI), sialic acid (SA) is used as a ligand to target the inflamed vascular endothelium. DXM-loaded SA-conjugated polyethylene glycol (PEG)ylated NPs (SA-NPs) are prepared via solvent diffusion method and show the good colloidal stability. SA-NPs reduce apoptotic human umbilical vein endothelial cells (HUVECs) via downregulating oxidative stress-induced Bax, upregulating Bcl-xL, and inhibiting Caspase-3 and Caspase-9 activation. Cellular uptake results suggest SA-NPs can be specifically internalized by the inflamed vascular endothelial cells (H O -pretreated HUVECs), and the mechanism is associated with the specific binding between SA and E-selectin receptor expressed on the inflamed vascular endothelial cells. Bio-distribution results further demonstrated the enhanced renal accumulation of DXM is achieved in AKI mice treated with SA-NPs, and its content is 2.70- and 5.88-fold higher than those treated with DXM and NPs at 6 h after intravenous administration, respectively. Pharmacodynamic studies demonstrate SA-NPs effectively ameliorate renal functions in AKI mice, as reflected by improved blood biochemical indexes, histopathological changes, oxidative stress levels and pro-inflammatory cytokines. Moreover, SA-NPs cause little negative effects on lymphocyte count and bone mineral density while DXM leads to severe osteoporosis. It is concluded that SA-NPs provide an efficient and targeted delivery of DXM for ischemia-reperfusion-induced injury-induced AKI, with improved therapeutic outcomes and reduced adverse effects.
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Portadores de Fármacos/química
Endotélio Vascular/efeitos dos fármacos
Lipídeos/química
Ácido N-Acetilneuramínico/química
Nanopartículas/química
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Animais
Caspase 3/metabolismo
Linhagem Celular
Dexametasona/farmacologia
Selectina E/metabolismo
Endotélio Vascular/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Nanopartículas/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
Polietilenoglicóis/química
Traumatismo por Reperfusão/metabolismo
Proteína X Associada a bcl-2/metabolismo
Proteína bcl-X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (E-Selectin); 0 (Lipids); 0 (bcl-2-Associated X Protein); 0 (bcl-X Protein); 30IQX730WE (Polyethylene Glycols); 7S5I7G3JQL (Dexamethasone); EC 3.4.22.- (Caspase 3); GZP2782OP0 (N-Acetylneuraminic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1410258


  10 / 13817 MEDLINE  
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[PMID]:29185784
[Au] Autor:Wang P; Guan Q; Zhou D; Yu Z; Song Y; Qiu W
[Ad] Endereço:1 Department of Oncology, Yantaishan Hospital , Yantai, China .
[Ti] Título:miR-21 Inhibitors Modulate Biological Functions of Gastric Cancer Cells via PTEN/PI3K/mTOR Pathway.
[So] Source:DNA Cell Biol;37(1):38-45, 2018 Jan.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gastric cancer is one of the most common malignancy in the world. microRNAs (miRNAs) are naturally occurring noncoding RNA that control gene expression by targeting messenger RNA (mRNA) for post-transcriptional repression or cleavage. This study focused on a specific miRNA, miR-21, which was overexpressed in gastric cancer and examined the effects of miR-21 inhibitor on biological functions of gastric cancer cells and its possible mechanism. Gastric cancer cells MKN74 were treated with miR-21 inhibitor, negative control, and blank control. Cell proliferation, colony formation, migration, and invasion were assessed. Real-time PCR and western blot were applied to examine the expression of phosphatase and tens in homolog deleted on chromosome ten (PTEN)/PI3K/mTOR pathway molecules. miR-21 inhibitor markedly suppressed proliferation, migration, invasion, and colony formation of gastric cancer cells. Anti-miR-21 treatment also reduced the expression ratio of B cell lymphoma 2 (Bcl-2)/Bax. Furthermore, miR-21 inhibition was associated with increased expression of PTEN, which in turn decreased the ratios of S235/236, S240/244, and p-AK/AKT in gastric cancer cells. Inhibiting miR-21 modulates biological functions of gastric cancer cells via PTEN/PI3K/mTOR pathway and miR-21 inhibitor may provide a novel therapeutic strategy for gastric cancer.
[Mh] Termos MeSH primário: MicroRNAs/genética
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Neoplasias Gástricas/genética
Serina-Treonina Quinases TOR/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Invasividade Neoplásica/genética
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
Transdução de Sinais/genética
Neoplasias Gástricas/patologia
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN21 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (bcl-2-Associated X Protein); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); 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); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3922



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