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[PMID]:29278024
[Au] Autor:Bardak H; Uguz AC; Bardak Y
[Ad] Endereço:1 Department of Ophthalmology, Haydarpasa Numune Research and Training Hospital , Istanbul, Turkey.
[Ti] Título:Curcumin regulates intracellular calcium release and inhibits oxidative stress parameters, VEGF, and caspase-3/-9 levels in human retinal pigment epithelium cells.
[So] Source:Physiol Int;104(4):301-315, 2017 Dec 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:In this study, we aimed to observe whether curcumin (cur), a polyphenolic compound derived from the dietary spice turmeric, a yellow substance obtained from the root of the plant Curcuma longa Linn, has any protective effect against blue light irradiation in human retinal pigment epithelium (ARPE-19) cells. For this purpose, we evaluated the intracellular calcium release mechanism, poly ADP ribose polymerase (PARP), procaspase-3/-9 protein expression levels, caspase activation, and reactive oxygen species levels. ARPE-19 cells were divided into four main groups, such as control, cur, blue light, and cur + blue light. Results were evaluated by Kruskal-Wallis and Mann-Whitney U tests as post hoc tests. The cells in cur and cur + blue light samples were incubated with 20 µM cur. Blue light exposure was performed for 24 h in an incubator. Lipid peroxidation and cytosolic-free Ca [Ca ] concentrations were higher in the blue light exposure samples than in the control samples; however, their levels were determined as significantly lower in the cur and cur + blue light exposure samples than in the blue light samples alone. PARP and procaspase-3 levels were significantly higher in blue light samples. Cur administration significantly decreased PARP and procaspase-3 expression levels. Reduced glutathione and glutathione peroxidase values were lower in the blue light exposure samples, although they were higher in the cur and cur + blue light exposure samples. Caspase-3 and -9 activities were lower in the cur samples than in the blue light samples. Moreover, vascular endothelial growth factor (VEGF) levels were significantly higher in the blue light exposure samples. In conclusion, cur strongly induced regulatory effects on oxidative stress, intracellular Ca levels, VEGF levels, PARP expression levels, and caspase-3 and -9 values in an experimental oxidative stress model in ARPE-19 cells.
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Caspase 3/metabolismo
Caspase 9/metabolismo
Curcumina/administração & dosagem
Epitélio Pigmentado da Retina/fisiologia
Fator A de Crescimento do Endotélio Vascular/metabolismo
Visão Ocular/fisiologia
[Mh] Termos MeSH secundário: Sinalização do Cálcio/efeitos dos fármacos
Sinalização do Cálcio/efeitos da radiação
Linhagem Celular
Relação Dose-Resposta a Droga
Seres Humanos
Luz
Estresse Oxidativo/fisiologia
Estresse Oxidativo/efeitos da radiação
Espécies Reativas de Oxigênio/metabolismo
Epitélio Pigmentado da Retina/efeitos dos fármacos
Epitélio Pigmentado da Retina/efeitos da radiação
Visão Ocular/efeitos dos fármacos
Visão Ocular/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9); IT942ZTH98 (Curcumin)
[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:171227
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.4.3


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[PMID]:29299551
[Au] Autor:Qi H; Jiang Y; Yin Z; Jiang K; Li L; Shuai J
[Ad] Endereço:Complex Systems Research Center, Shanxi University, Taiyuan 030006, China.
[Ti] Título:Optimal pathways for the assembly of the Apaf-1·cytochrome c complex into apoptosome.
[So] Source:Phys Chem Chem Phys;20(3):1964-1973, 2018 Jan 17.
[Is] ISSN:1463-9084
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The formation of a heptameric apoptosome is a crucial event in the intrinsic cell death pathway. Considerable progress has been made towards unraveling the constituents and the structure of the apoptosome as well as the mechanism of apoptosome-mediated caspase-9 activation. However, a significant gap remains in the understanding of this process, i.e., how seven Apaf-1·cytochrome c complexes stepwisely assemble into an apoptosome. Here, we construct a biophysical model that incorporates current biochemical knowledge about the formation of apoptosome. We propose 11 elementary routes and enumerate all 2047 possible assembly pathways from the Apaf-1·cytochrome c complex to the heptameric apoptosome. By combining mathematical analysis and numerical simulation, we find that two elementary routes are the most favorable biochemical reaction routes and there are 52 optimal assembly pathways which are economical and relatively fast. Our study yields the first comprehensive analysis of apoptosome assembly and provides insights into complex assembly pathways.
[Mh] Termos MeSH primário: Apoptossomas/metabolismo
Fator Apoptótico 1 Ativador de Proteases/metabolismo
Caspase 9/metabolismo
[Mh] Termos MeSH secundário: Apoptossomas/química
Fator Apoptótico 1 Ativador de Proteases/química
Citocromos c/metabolismo
Seres Humanos
Cinética
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APAF1 protein, human); 0 (Apoptosomes); 0 (Apoptotic Protease-Activating Factor 1); 9007-43-6 (Cytochromes c); EC 3.4.22.- (Caspase 9)
[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:180105
[St] Status:MEDLINE
[do] DOI:10.1039/c7cp06726g


  3 / 5921 MEDLINE  
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[PMID]:29309885
[Au] Autor:Fei HR; Li ZJ; Ying-Zhang; Yue-Liu; Wang FZ
[Ad] Endereço:School of Pharmacology, Taishan Medical University, Chang Cheng Road, Taian 271016, PR China.
[Ti] Título:HBXIP regulates etoposide-induced cell cycle checkpoints and apoptosis in MCF-7 human breast carcinoma cells.
[So] Source:Gene;647:39-47, 2018 Mar 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Etoposide, an anticancer DNA topoisomerase II poison, plays an important role in the therapy for human cancers. Unfortunately, many cancers develop etoposide resistance and do not respond to chemotherapy, leading to difficulty in treatment and poor prognosis. In this study, we investigate the effects of HBXIP gene silencing on etoposide chemosensitivity in MCF-7 human breast cancer cells. We find that etoposide increases HBXIP expression and promotes mobilization of HBXIP to the nucleus in MCF-7 cells. Knockdown of HBXIP alleviates etoposide-induced G2/M or S phase arrest. Upregulation of p53 and p21 upon etoposide treatment is attenuated in HBXIP knock-down cells. Moreover, HBXIP gene silencing sensitizes etoposide-induced cell apoptosis and cleavage of caspase-9 and PARP in MCF-7 cells. Knockdown of HBXIP expression by RNAi abrogates the etoposide-activated ERK and Akt. These results indicate that HBXIP can modulate the etoposide sensitivity of MCF-7 cell lines and further implicate HBXIP as a target for human breast cancer.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Apoptose/efeitos dos fármacos
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Etoposídeo/farmacologia
[Mh] Termos MeSH secundário: Caspase 9/metabolismo
Linhagem Celular Tumoral
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Feminino
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Células MCF-7
Poli(ADP-Ribose) Polimerases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteína Supressora de Tumor p53/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (HBXIP protein, human); 0 (Tumor Suppressor Protein p53); 6PLQ3CP4P3 (Etoposide); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  4 / 5921 MEDLINE  
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[PMID]:29254330
[Au] Autor:Shi H; Zou J; Zhang T; Che H; Gao X; Wang C; Wang Y; Xue C
[Ad] Endereço:College of Food Science and Engineering, Ocean University of China , No. 5 Yushan Road, Qingdao, Shandong Province 266003, PR China.
[Ti] Título:Protective Effects of DHA-PC against Vancomycin-Induced Nephrotoxicity through the Inhibition of Oxidative Stress and Apoptosis in BALB/c Mice.
[So] Source:J Agric Food Chem;66(2):475-484, 2018 Jan 17.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The clinical use of glycopeptide antibiotic vancomycin is usually accompanied by nephrotoxicity, limiting its application and therapeutic efficiency. The aim of this study was to investigate the protection of DHA-enriched phosphatidylcholine (DHA-PC) against nephrotoxicity using a model of vancomycin-induced male BALB/c mice with renal injury by measuring death curves, histological changes, and renal function indexes. The addition of DHA in DHA and DHA-PC groups were 300 mg/kg per day on the basis of human intake level in our study. Results indicated that DHA-PC could dramatically extend the survival time of mice, while traditional DHA and PC had no significant effects. Moreover, oral administration of DHA-PC exhibited better effects on reducing vancomycin-induced increases of blood urea nitrogen, creatinine, cystatin C, and kidney injury molecule-1 levels than traditional DHA and PC. DHA-PC significantly delayed the development of vancomycin-induced renal injury, including tubular necrosis, hyaline casts, and tubular degeneration. A further mechanistic study revealed that the protective effect of DHA-PC on vancomycin-mediated toxicity might be attributed to its ability to inhibit oxidative stress and inactivate mitogen-activated protein kinase (MAPK) signaling pathways, which was associated with upregulation of Bcl-2 and downregulation of caspase-9, caspase-3, cytochrome-c, p38, and JNK. These findings suggest that DHA-PC may be acted as the dietary supplements or functional foods against vancomycin-induced nephrotoxicity.
[Mh] Termos MeSH primário: Antibacterianos/toxicidade
Apoptose/efeitos dos fármacos
Ácidos Docosa-Hexaenoicos/administração & dosagem
Nefropatias/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilcolinas/administração & dosagem
Substâncias Protetoras/administração & dosagem
Vancomicina/toxicidade
[Mh] Termos MeSH secundário: Animais
Caspase 3/genética
Caspase 3/metabolismo
Caspase 9/genética
Caspase 9/metabolismo
Citocromos c/metabolismo
Ácidos Docosa-Hexaenoicos/química
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/fisiopatologia
Nefropatias/etiologia
Nefropatias/genética
Nefropatias/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Proteínas Quinases Ativadas por Mitógeno/genética
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fosfatidilcolinas/química
Substâncias Protetoras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Phosphatidylcholines); 0 (Protective Agents); 25167-62-8 (Docosahexaenoic Acids); 6Q205EH1VU (Vancomycin); 9007-43-6 (Cytochromes c); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04565


  5 / 5921 MEDLINE  
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[PMID]:29179205
[Au] Autor:Liu H; Jing X; Dong A; Bai B; Wang H
[Ad] Endereço:Department of Cardiology, Tangdu Hospital, the Fourth Military University, Xi'an, China.
[Ti] Título:Overexpression of TIMP3 Protects Against Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Apoptosis Through ROS/Mapks Pathway.
[So] Source:Cell Physiol Biochem;44(3):1011-1023, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Myocardial ischemia/reperfusion (I/R) injury remains a great challenge in clinical therapy. Tissue inhibitor of metalloproteinases 3 (TIMP3) plays a crucial role in heart physiological and pathophysiological processes. However, the effects of TIMP3 on I/R injury remain unknown. METHODS: C57BL/6 mice were infected with TIMP3 adenovirus by local delivery in myocardium followed by I/R operation or doxorubicin treatment. Neonatal rat cardiomyocytes were pretreated with TIMP3 adenovirus prior to anoxia/reoxygenation (A/R) treatment in vitro. Histology, echocardiography, in vivo phenotypical analysis, flow cytometry and western blotting were used to investigate the altered cardiac function and underlying mechanisms. RESULTS: The results showed that upregulation of TIMP3 in myocardium markedly inhibited myocardial infarct areas and the cardiac dysfunction induced by I/R or by doxorubicin treatment. TUNEL staining revealed that TIMP3 overexpression attenuated I/R-induced myocardial apoptosis, accompanied by decreased Bax/Bcl-2 ratio, Cleaved Caspase-3 and Cleaved Caspase-9 expression. In vitro, A/R-induced cardiomyocyte apoptosis was abrogated by pharmacological inhibition of reactive oxygen species (ROS) production or MAPKs signaling. Attenuation of ROS production reversed A/R-induced MAPKs activation, whereas MAPKs inhibitors showed on effect on ROS production. Furthermore, in vivo or in vitro overexpression of TIMP3 significantly inhibited I/R- or A/R-induced ROS production and MAPKs activation. CONCLUSION: Our findings demonstrate that TIMP3 upregulation protects against cardiac I/R injury through inhibiting myocardial apoptosis. The mechanism may be related to inhibition of ROS-initiated MAPKs pathway. This study suggests that TIMP3 may be a potential therapeutic target for the treatment of I/R injury.
[Mh] Termos MeSH primário: Miocárdio/metabolismo
Inibidor Tecidual de Metaloproteinase-3/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Antracenos/farmacologia
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Caspase 9/metabolismo
Células Cultivadas
Óxidos N-Cíclicos/farmacologia
Doxorrubicina/toxicidade
Ecocardiografia
Coração/diagnóstico por imagem
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Traumatismo por Reperfusão Miocárdica/induzido quimicamente
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Marcadores de Spin
Inibidor Tecidual de Metaloproteinase-3/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Cyclic N-Oxides); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (Spin Labels); 0 (Tissue Inhibitor of Metalloproteinase-3); 0 (bcl-2-Associated X Protein); 1TW30Y2766 (pyrazolanthrone); 80168379AG (Doxorubicin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9); U78ZX2F65X (tempol); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485401


  6 / 5921 MEDLINE  
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[PMID]:29037999
[Au] Autor:Aykac A; Karanlik B; Sehirli AO
[Ad] Endereço:Near East University, Faculty of Medicine, Department of Biophysics, Nicosia, Cyprus.
[Ti] Título:Protective effect of silk fibroin in burn injury in rat model.
[So] Source:Gene;641:287-291, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Activation of pro-inflamatuar pathways play major role in formation of major complications as a result of burns. This study was planned to investigate the protective effect of Silk Fibroin in lung injury caused by burn in the experimental rat model. After rinsing the skin of rats under ether anesthesia, the exposed back region, covers 30% of the total body, was kept in the 90°C water bath for 10s. The control rats were kept in the 25°C water bath for 10s. Immediately after burning process, silk fibroin was administered orally at a dose of 600mg/kg. After 24h following burning from all groups the levels of TNF-α, IL-1ß in blood samples and the MDA, GSH and the activity of MPO were determined from taken lung tissues. Moreover, the expression of Bcl-2/Bax, Caspase-3 and Caspase-9 were determined. Significant increase in TNF-α, IL-1ß, Casp-3 and Casp-9 levels were observed in the Silk Fibroin-treated burn group (p<0.05) whereas for ratio of Bcl-2/Bax, a significant reduction was observed compared to control group (p<0.05). Increased levels of TNF-α, IL-1ß, Caspase-3 and Caspase-9 in Silk Fibroin-treated burn groups were found to be reversed. Silk fibroin can be an effective biomaterial in diminishing burn injury in tissue and apoptosis.
[Mh] Termos MeSH primário: Bombyx/metabolismo
Queimaduras/tratamento farmacológico
Fibroínas/farmacologia
Lesão Pulmonar/tratamento farmacológico
Substâncias Protetoras/farmacologia
Seda/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Caspase 9/metabolismo
Modelos Animais de Doenças
Feminino
Interferon-alfa/metabolismo
Interleucina-1beta/metabolismo
Lesão Pulmonar/metabolismo
Masculino
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos
Ratos Wistar
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon-alpha); 0 (Interleukin-1beta); 0 (Protective Agents); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Silk); 0 (bcl-2-Associated X Protein); 0 (fibroin, silkworm); 9007-76-5 (Fibroins); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


  7 / 5921 MEDLINE  
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[PMID]:27777194
[Au] Autor:Huang H; Tian ZT; Yao YM; Li TS
[Ad] Endereço:1Emergency Department, Chinese PLA General Hospital, Beijing 100853, China; 2Department of Critical Care Medicine, General Hospital of Jinan Command, Jinan 250031, China. E-mail: huanghe_hh@126.com.
[Ti] Título:[Tumor necrosis factor-α-induced protein 8 like-2 promotes apoptosis of CD4 T lymphocytes in mice with severe burn injury].
[So] Source:Nan Fang Yi Ke Da Xue Xue Bao;36(10):1334-1339, 2016 Oct 20.
[Is] ISSN:1673-4254
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the effect of tumor necrosis factor-α-induced protein 8 like-2 (TIPE2) on apoptosis of CD4 T lymphocytes in a murine model of severe burn injury. METHODS: A total of 140 male mice were randomly allocated into 6 groups. Small RNA interference technique was used to construct a siTIPE2-overexpressing lentivirus, and severe burn injury models were established in the mice. CD4 T cells were purified from spleen of the mice, and the expressions of TIPE2, Smad2/Smad3, P-Smad2/P-Smad3 and Bcl-2/Bimprotein in CD4 Tregs were detected. The changes in mitochondrial membrane potential and cytochrome C in CD4 T cells were detected, and the activities of caspase-3, caspase-8, and caspase-9 were analyzed. RESULTS: Down-regulation of TIPE2 promoted the apoptosis of CD4 T lymphocytes in siTIPE2-burn group, in which the protein expressions of P-smad2/P-Smad3 decreased, Bcl-2 expression increased and Bim expression decreased significantly as compared with the other groups (P<0.01 or 0.05). The mitochondrial membrane potential and cytochrome C expression in CD4 T cells were down-regulated in siTIPE2-burn group (P<0.05) with a lowered caspase-3 activity compared with TIPE2-burn group (P<0.01) and decreased caspase-8 and caspase-9 compared with the other groups (P<0.05). The apoptosis rate was the highest in TIPE2-burn group, whose Smad2/Smad3 was higher than that in the sham group (P<0.05) and the expression of P-smad2/P-Smad3 significantly increased compared with the other groups (P<0.05). In TIPE2-burn group, the mitochondrial membrane potential in CD4 T cells was decreased (P<0.01), the expression of cytochrome C increased markedly (P<0.01), and the activities of caspase-3, caspase-8, and caspase-9 were all obviously higher than those in the other groups (P<0.05). CONCLUSION: As an important immunoregulatory molecule, TIPE2 can promote the apoptosis of CD4 T lymphocyte in mice with sever burn injury.
[Mh] Termos MeSH primário: Apoptose
Queimaduras/imunologia
Linfócitos T CD4-Positivos/citologia
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
[Mh] Termos MeSH secundário: Animais
Caspase 3/metabolismo
Caspase 8/metabolismo
Caspase 9/metabolismo
Regulação para Baixo
Masculino
Camundongos
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Baço
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); 0 (Smad2 Protein); 0 (Smad2 protein, mouse); 0 (Smad3 Protein); 0 (Smad3 protein, mouse); 0 (TIPE2 protein, mouse); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Casp8 protein, mouse); EC 3.4.22.- (Casp9 protein, mouse); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 8); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  8 / 5921 MEDLINE  
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[PMID]:29061809
[Au] Autor:Maiuthed A; Pinkhien T; Chamni S; Suwanborirux K; Saito N; Petpiroon N; Chanvorachote P
[Ad] Endereço:Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
[Ti] Título:Apoptosis-inducing Effect of Hydroquinone 5- -Cinnamoyl Ester Analog of Renieramycin M on Non-small Cell Lung Cancer Cells.
[So] Source:Anticancer Res;37(11):6259-6267, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A newly-synthesized derivative of renieramycin M (RM), an anticancer lead compound isolated from the blue sponge Xestospongia sp., hydroquinone 5-O-cinnamoyl ester (CIN-RM), was investigated here for its activity against non-small cell lung cancer cells. MATERIALS AND METHODS: Cytotoxicity effects of CIN-RM and RM on H292 lung cancer cells were determined by the MTT assay. We also investigated the mechanism of CIN-RM-mediated apoptosis and mechanism of action of this compound by western blotting. RESULTS: CIN-RM showed more potent cytotoxicity than its parental compound (RM) against H292 lung cancer cells. At concentrations of 15-60 µM, CIN-RM significantly induced apoptosis by increasing expression of apoptosis-inducing factor (AIF) and activation of caspase-3 and -9. For up-stream mechanism, CIN-RM mediated apoptosis through a p53-dependent mechanism, that consequently down-regulated anti-apoptotic B-cell lymphoma 2 (BCL2), while increasing the level of pro-apoptotic BCL2-associated X (BAX). In addition, phosphorylation of pro-survival protein AKT was found to be dramatically reduced. CONCLUSION: This study revealed the potential of CIN-RM for apoptosis induction and in the development of a novel anticancer agent.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Hidroquinonas/farmacologia
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Fator de Indução de Apoptose/metabolismo
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Caspase 3/metabolismo
Caspase 9/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Hidroquinonas/síntese química
Hidroquinonas/química
Neoplasias Pulmonares/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Tetra-Hidroisoquinolinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIFM1 protein, human); 0 (Apoptosis Inducing Factor); 0 (Hydroquinones); 0 (Tetrahydroisoquinolines); 0 (renieramycin M); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP9 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  9 / 5921 MEDLINE  
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[PMID]:29034805
[Au] Autor:Vural K; Kosova F; Kurt FÖ; Tuglu I
[Ad] Endereço:1 Department of Medical Pharmacology, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.
[Ti] Título:In vitro investigation of the effect of matrix molecules on the behavior of colon cancer cells under the effect of geldanamycin derivative.
[So] Source:Tumour Biol;39(10):1010428317720569, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chaperone-binding drug, 17-allylamino-17-demethoxygeldanamycin, has recently come into clinical use. It is a derivative of geldanamycin, an ansamycin benzoquinone antibiotic with anti-carcinogenic effect. Understanding the effect of this drug on the cancer cells and their niche is important for treatment. We applied 17-allylamino-17-demethoxygeldanamycin to colon cancer cell line (Colo 205) on matrix molecules to investigate the relationship of apoptosis with terminal deoxynucleotidyl transferase dUTP nick end labeling immunocytochemistry and related gene expression. We used laminin and collagen I for matrix molecules and vascular endothelial growth factor for angiogenic structure. We also examined apoptosis-related signaling pathway including mitochondrial proteins, cytochrome c, Bcl-2, caspase-9, Apaf-1 expression using real-time polymerase chain reaction. There was clear effect of 17-allylamino-17-demethoxygeldanamycin that killed more cells on tissue culture plastic compared to matrix molecules. The IC value was 0.58 µg/mL for tissue culture plastic compared with 0.64 µg/mL for laminin and 0.75 µg/mL for collagen I. The analyses showed that more cells on matrix molecules underwent apoptosis compared to that on tissue culture plastic. Apoptosis-related gene expression was similar in which Bcl-2 expression decreased and proapoptotic gene expression of the cells on matrix molecules increased compared to that on tissue culture plastic. However, the application of 17-allylamino-17-demethoxygeldanamycin was more effective for the cells on collagen I compared to the cells on laminin. There was also a decrease in angiogenesis as shown by the vascular endothelial growth factor staining. This was more pronounced by coating of the tissue culture plastic with matrix molecules. Our results supported the anti-cancer effect of 17-allylamino-17-demethoxygeldanamycin, and this effect depended on matrix molecules. This effect occurs through apoptosis, and related genes were also altered. All these genes may serve for novel target under the effect of matrix substrate. However, correct interpretation of the results requires further studies.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Benzoquinonas/farmacologia
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/metabolismo
Lactamas Macrocíclicas/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Fator Apoptótico 1 Ativador de Proteases/metabolismo
Caspase 9/metabolismo
Linhagem Celular Tumoral
Colágeno/metabolismo
Colo/efeitos dos fármacos
Colo/metabolismo
DNA Nucleotidilexotransferase/metabolismo
Seres Humanos
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Rifabutina/farmacologia
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Apoptotic Protease-Activating Factor 1); 0 (Benzoquinones); 0 (Lactams, Macrocyclic); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Vascular Endothelial Growth Factor A); 1W306TDA6S (Rifabutin); 3T006GV98U (quinone); 4GY0AVT3L4 (tanespimycin); 9007-34-5 (Collagen); EC 2.7.7.31 (DNA Nucleotidylexotransferase); EC 3.4.22.- (Caspase 9); Z3K3VJ16KU (geldanamycin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317720569


  10 / 5921 MEDLINE  
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[PMID]:28945745
[Au] Autor:Napoletano F; Gibert B; Yacobi-Sharon K; Vincent S; Favrot C; Mehlen P; Girard V; Teil M; Chatelain G; Walter L; Arama E; Mollereau B
[Ad] Endereço:Laboratory of Biology and Modelling of the Cell, UMR5239 CNRS/Ecole Normale Supérieure de Lyon, INSERM U1210, UMS 3444 Biosciences Lyon Gerland, Université de Lyon, Lyon, France.
[Ti] Título:p53-dependent programmed necrosis controls germ cell homeostasis during spermatogenesis.
[So] Source:PLoS Genet;13(9):e1007024, 2017 Sep.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The importance of regulated necrosis in pathologies such as cerebral stroke and myocardial infarction is now fully recognized. However, the physiological relevance of regulated necrosis remains unclear. Here, we report a conserved role for p53 in regulating necrosis in Drosophila and mammalian spermatogenesis. We found that Drosophila p53 is required for the programmed necrosis that occurs spontaneously in mitotic germ cells during spermatogenesis. This form of necrosis involved an atypical function of the initiator caspase Dronc/Caspase 9, independent of its catalytic activity. Prevention of p53-dependent necrosis resulted in testicular hyperplasia, which was reversed by restoring necrosis in spermatogonia. In mouse testes, p53 was required for heat-induced germ cell necrosis, indicating that regulation of necrosis is a primordial function of p53 conserved from invertebrates to vertebrates. Drosophila and mouse spermatogenesis will thus be useful models to identify inducers of necrosis to treat cancers that are refractory to apoptosis.
[Mh] Termos MeSH primário: Necrose/genética
Espermatogênese/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Caspase 9/genética
Caspases/genética
Modelos Animais de Doenças
Proteínas de Drosophila/genética
Drosophila melanogaster/genética
Drosophila melanogaster/crescimento & desenvolvimento
Células Germinativas/crescimento & desenvolvimento
Células Germinativas/patologia
Homeostase/genética
Seres Humanos
Hiperplasia/genética
Hiperplasia/patologia
Masculino
Camundongos
Necrose/patologia
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Tumor Suppressor Protein p53); EC 3.4.22.- (Caspase 9); EC 3.4.22.- (Caspases); EC 3.4.22.- (Nc protein, Drosophila)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007024



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