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[PMID]:29446584
[Au] Autor:Sosedova LM; Novikov MA; Titov EA; Rukavishnikov VS
[Ti] Título:[Induction of apoptosis in neurons of white rats under exposure of nanobiocomposite based on ag (0) nanoparticles and arabinogalactan].
[So] Source:Gig Sanit;95(12):1210-13, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:There are presented results of the immunohistochemical study of neural tissue of outbred albino rats exposed for 9 days to the influence of the silver nanobiocomposite consisted of silver nanoparticles encapsulated into a matrix of a natural polymer - arabinogalactan. The research of albino rats was performed in 2 stages: half of the rats in each groups were decapitated immediately after the exposure (early period) and the rest animals - 6 months after the end of exposure (remote period). The impact of the studied substance was proved to cause functional changes in cells of the nervous tissue. After the subacute administration of the nanobiocomposite - argentum-arabinogalactan (nano-Ag-AG) in cells of the nervous tissue of the brain of albino rats the expression of apoptotic and anti-apoptotic protein (caspase-3 and bcl-2) was established to be changed. The number of normal neurons producing protein caspase-3 sharply increases. Herewith the number of immunonegative neurons fairly declines. Along with this there is noted the high level of bcl-2 content, one function ofwhich is the preclusion ofapoptosis. In preparations there is revealed a significant gain in the number of bcl-2 expressing neurons, however, the protective effect of the protein is not fully realized, that leads to the significantly increase in the content of damaged hyperchromatic cells. The evaluation of results of the immunohistochemical study of the nervous tissue of albino rats according to data concerning the proteins caspase-3 and bcl-2 expression permits to make a conclusion about the capability of nanoargentum encapsulated into polymer matrix by passing the blood-brain barrier to induce the triggering apoptosis cascade in neurons of the cerebral cortex.
[Mh] Termos MeSH primário: Encéfalo
Galactanos/farmacologia
Larix
Nanopartículas Metálicas/efeitos adversos
Prata
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Biopolímeros/farmacologia
Barreira Hematoencefálica/metabolismo
Encéfalo/efeitos dos fármacos
Encéfalo/patologia
Encéfalo/fisiopatologia
Caspase 3/metabolismo
Imuno-Histoquímica
Modelos Animais
Preparações de Plantas/farmacologia
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos
Prata/efeitos adversos
Prata/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biopolymers); 0 (Galactans); 0 (Plant Preparations); 0 (Proto-Oncogene Proteins c-bcl-2); 3M4G523W1G (Silver); EC 3.4.22.- (Caspase 3); SL4SX1O487 (arabinogalactan)
[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:180216
[St] Status:MEDLINE


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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]:28456679
[Au] Autor:Khaliq NU; Oh KS; Sandra FC; Joo Y; Lee J; Byun Y; Kim IS; Kwon IC; Seo JH; Kim SY; Yuk SH
[Ad] Endereço:College of Pharmacy, Korea University, 2511 Sejongro, Sejong 30019, Republic of Korea.
[Ti] Título:Assembly of polymer micelles through the sol-gel transition for effective cancer therapy.
[So] Source:J Control Release;255:258-269, 2017 Jun 10.
[Is] ISSN:1873-4995
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Photo-induced apoptosis-targeted chemotherapy (PIATC) was designed and characterized to propose a new protocol for improved chemotherapy. Intratumoral injection was selected as the mode of administration of the anticancer drug, doxorubicin (DOX). To extend the retention time of DOX at the tumor parenchyma, in-situ gel formation was induced through the sol-gel transition of the Pluronic NPs containing a prodrug of DOX or a photosensitizer. The prodrug (DEVD-S-DOX) was designed to be inactive with a peptide moiety (Aspartic acid-Glutamic acid-Valine-Aspartic acid: DEVD) linked to DOX and to be cleaved into free DOX by caspase-3 expressed with apoptosis. For reactive oxygen species (ROS)-mediated apoptosis, photo-irradiation with methylene blue (MB, photosensitizer) was utilized. The sol-gel transition of the Pluronic NPs containing reactive species, DEVD-S-DOX or MB, was examined by measuring the cloud point and the gel strength in response to temperature change. ROS-mediated apoptosis was observed by measuring the ROS and membrane integrity with induced apoptosis. The in vivo antitumor efficacy of PIATC was measured with a cardiotoxicity assay in tumor-bearing mice.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Doxorrubicina/administração & dosagem
Azul de Metileno/administração & dosagem
Fotoquimioterapia
Fármacos Fotossensibilizantes/administração & dosagem
Poloxâmero/administração & dosagem
Pró-Fármacos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacocinética
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Linhagem Celular Tumoral
Doxorrubicina/farmacocinética
Doxorrubicina/uso terapêutico
Liberação Controlada de Fármacos
Géis
Luz
Masculino
Azul de Metileno/uso terapêutico
Camundongos Endogâmicos C3H
Micelas
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Fármacos Fotossensibilizantes/uso terapêutico
Poloxâmero/uso terapêutico
Pró-Fármacos/farmacocinética
Pró-Fármacos/uso terapêutico
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Gels); 0 (Micelles); 0 (Photosensitizing Agents); 0 (Prodrugs); 0 (Reactive Oxygen Species); 106392-12-5 (Poloxamer); 80168379AG (Doxorubicin); EC 3.4.22.- (Caspase 3); T42P99266K (Methylene Blue)
[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:170501
[St] Status:MEDLINE


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[PMID]:29205963
[Au] Autor:Li F; Zhang Y; Ma SL
[Ad] Endereço:School of Forensic Medicine, Henan University of Science and Technology, Luoyang 471003, China.
[Ti] Título:[Relationship between the Expression of α-syn and Neuronal Apoptosis in Brain Cortex of Acute Alcoholism Rats].
[So] Source:Fa Yi Xue Za Zhi;32(6):406-409, 2016 Dec.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To observe the changes of expression of α-synuclein (α-syn) and neuronal apoptosis in brain cortex of acute alcoholism rats and to explore the mechanism of the damage caused by ethanol to the neurons. METHODS: The model of acute alcoholism rat was established by 50% alcohol gavage. The α-syn and caspase-3 were detected by immunohistochemical staining and imaging analysis at 1 h, 3 h, 6 h and 12 h after acute alcoholism. The number of positive cell and mean of optical density were detected and the trend change was analyzed. The variance analysis and -test were also performed. RESULTS: The number of α-syn positive cell and average optical density in brain cortex of acute alcoholism rat increased significantly and peaked at 6 hour with a following slight decrease at 12 h, but still higher than the groups at 1 h and 3 h. Within 12 hours after poisoning, the number of caspase-3 positive cell and average optical density in brain cortex of rats gradually increased. CONCLUSIONS: The abnormal aggregation of α-syn caused by brain edema and hypoxia may participate the early stage of neuronal apoptosis in brain cortex after acute alcoholism.
[Mh] Termos MeSH primário: Alcoolismo/patologia
Apoptose
Córtex Cerebral/patologia
Neurônios/patologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Alcoolismo/metabolismo
Animais
Edema Encefálico/patologia
Caspase 3/metabolismo
Córtex Cerebral/metabolismo
Etanol
Hipóxia/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Synuclein); 3K9958V90M (Ethanol); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.06.002


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[PMID]:29374923
[Au] Autor:Bai XZ; He T; Zhang JL; Liu Y; Cao MY; Zhang JN; Cai WX; Jia YH; Shi JH; Su LL; Hu DH
[Ad] Endereço:Burn Center of PLA, Department of Burns and Cutaneous Surgery, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
[Ti] Título:[Effects of microRNA-34a on regulating silent information regulator 1 and influence of the factor on myocardial damage of rats with severe burns at early stage].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):21-28, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the effects of microRNA-34a on regulating silent information regulator 1 (SIRT1) and influence of SIRT1 on myocardial damage of rats with severe burns at early stage. (1) Twenty-four Sprague-Dawley (SD) rats were divided into sham injury (SI) group, simple burns (SB) group and SIRT1 agonist (SA) group according to the random number table (the same grouping method below), with 8 rats in each group. Rats in groups SB and SA were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns) on the back, and rats in group SI were sham injuried on the back. Immediately after injury, rats in groups SI and SB were intraperitoneally injected with normal saline of 50 mL/kg, and rats in group SA were intraperitoneally injected with normal saline of 50 mL/kg and 1 mg/mL resveratrol of 50 mg/kg. At 6 h post injury, abdominal aortic blood was collected to make serum and myocardial tissue of rats was collected. (2) Myocardial cells of twelve neonatal SD rats were collected and divided into microRNA-34a mimic control (MMC) group, microRNA-34a mimic (MM) group, microRNA-34a inhibitor control (MIC) group, and microRNA-34a inhibitor (MI) group, which were respectively transfected with gene sequences of mimic control, mimic, inhibitor control, and inhibitor of microRNA-34a. The microRNA-34a expression level and protein expression level of SIRT1 in myocardial cells were respectively detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Another batch of myocardial cells were divided into microRNA-34a inhibitor control+ burn serum (MCB) group, microRNA-34a inhibitor+ burn serum (MB) group, and microRNA-34a inhibitor+ burn serum + EX527 (MBE) group. Myocardial cells in group MCB were transfected with gene sequence of inhibitor control, and myocardial cells in the later groups were transfected with gene sequence of inhibitor of microRNA-34a. After transfection of 48 h, myocardial cells in group MBE were cultured in Dulbecco's modified Eagle's medium (DMEM) solution for 6 hours, with serum in group SB of volume fraction of 10% and final amount-of-substance concentration of 1 mol/L, and myocardial cells in the other 2 groups were cultured in DMEM solution with serum from rats of group SB of volume fraction of 10%. The protein expression levels of myocardial cells of SIRT1, cleaved-caspase-3, and Bax were detected by Western blotting. (3) Myocardial tissue from (1) was collected to detect expression levels of microRNA-34a and mRNA of SIRT1 in groups SI and SB by real-time fluorescence quantitative RT-PCR. Morphology of myocardial tissue of rats in groups SI, SB, and SA was observed with biological image navigator. The mRNA expression levels of interleukin 1ß (IL-1ß) and tumor necrosis factor (TNF-α) of rats in groups SI, SB, and SA were detected by real-time fluorescence quantitative RT-PCR. The expression levels of cleaved-caspase-3, and Bax of myocardial tissue of rats in groups SI, SB, and SA were detected by Western blotting. Data were processed with one-way analysis of variance and least-significant difference test. (1) After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MM was 4.67±0.92, significantly higher than 1.03±0.04 in group MMC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MM was 0.35±0.06, significantly lower than 1.12±0.11 in group MMC ( <0.01). After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MI was 0.26±0.07, significantly lower than 1.33±0.07 in group MIC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MIC was 1.12±0.16, significantly lower than 1.74±0.34 in group MI ( <0.01). At 6 h after culture, compared with those in group MCB, the SIRT1 protein expression level of myocardial cells in group MB was significantly increased ( <0.05), while cleaved-caspase-3 and Bax protein expression levels of myocardial cells in group MB were significantly decreased ( <0.05). Compared with those in group MB, the SIRT1 protein expression level of myocardial cells in group MBE was with no significantly statistical difference ( >0.05), and cleaved-caspase-3 and Bax protein expression levels were significantly increased ( <0.05). (2) At 6 h post injury, compared with that in group SI, the microRNA-34a expression level of myocardial tissue in group SB was significantly increased ( <0.01), and the mRNA expression level of SIRT1 of myocardial tissue in group SB was significantly decreased ( <0.01). At 6 h post injury, myocardial cells in group SI arranged neatly with normal nucleus and no inflammatory cells infiltration; myocardial cells in group SB arranged disorderly, with no abnormal nucleus, and obvious inflammatory cells infiltration; myocardial cells in group SA arranged neatly, with normal nucleus and little inflammatory cells infiltration. At 6 h post injury, compared with those in group SB, the mRNA expression levels of IL-1ß and TNF-α, and the protein expression levels of cleaved-caspase-3 and Bax of myocardial tissue in groups SI and SA were significantly decreased ( <0.01). The microRNA-34a expression level of myocardial tissue of rats with severe burns at early stage increases, which decreases the expression level of SIRT1, and increases the expression levels of IL-1ß, TNF-α, cleaved-caspase-3 and Bax, leading to obvious myocardial damage. Activation of SIRT1 can alleviate myocardial damage of rats with severe burns at early stage through decreasing expression levels of IL-1ß, TNF-α, cleaved-caspase-3, and Bax.
[Mh] Termos MeSH primário: Queimaduras
MicroRNAs/genética
Miocárdio/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Caspase 3/genética
Caspase 3/metabolismo
Interleucina-1beta
Miocárdio/patologia
Miócitos Cardíacos
RNA Mensageiro/genética
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Sirtuína 1/genética
Estilbenos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Stilbenes); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 3); EC 3.5.1.- (Sirt1 protein, rat); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[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:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.005


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[PMID]:29421518
[Au] Autor:Luo H; Liang H; Chen Y; Chen S; Xu Y; Xu L; Liu J; Zhou K; Peng J; Guo G; Lai B; Song L; Yang H; Liu L; Peng J; Liu Z; Tang L; Chen W; Tang H
[Ad] Endereço:Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
[Ti] Título:miR-7-5p overexpression suppresses cell proliferation and promotes apoptosis through inhibiting the ability of DNA damage repair of PARP-1 and BRCA1 in TK6 cells exposed to hydroquinone.
[So] Source:Chem Biol Interact;283:84-90, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hydroquinone (HQ), one of the major metabolic products of benzene, is a carcinogen, which induces apoptosis and inhibit proliferation in lymphoma cells. microRNA-7-5p (miR-7-5p), a tumor suppressor, participates in various biological processes including cell proliferation and apoptosis regulation by repressing expression of specific oncogenic target genes. To explore whether miR-7-5p is involved in HQ-induced cell proliferation and apoptosis, we assessed the effect of miR-7-5p overexpression on induction of apoptosis analyzed by FACSCalibur flow cytometer in transfection of TK6 cells with miR-7-5p mimic (TK6- miR-7-5p). We observed an increased apoptosis by 25.43% and decreased proliferation by 28.30% in TK6-miR-7-5p cells compared to those negative control cells (TK6-shNC) in response to HQ treatment. Furthermore, HQ might active the apoptotic pathway via partly downregulation the expression of BRCA1 and PARP-1, followed by p53 activation, in TK6-miR-7-5p cells. In contrast, attenuated p53 and BRCA1 expression was observed in shPARP-1 cells than in NC cells after HQ treatment. Therefore, we conclude that HQ may activate apoptotic signals via inhibiting the tumor suppressive effects of miR-7-5p, which may be mediated partly by upregulating the expression of PARP-1 and BRCA1 in control cells. The increase of miR-7-5p expression further intensified downregulation of PARP-1 and BRCA1 in TK6-miR-7-5p cells, resulting in an increase of apoptosis and proliferation inhibited.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína BRCA1/metabolismo
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Hidroquinonas/farmacologia
MicroRNAs/metabolismo
Poli(ADP-Ribose) Polimerase-1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Antagomirs/metabolismo
Proteína BRCA1/genética
Caspase 3/metabolismo
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Seres Humanos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Poli(ADP-Ribose) Polimerase-1/genética
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Hydroquinones); 0 (MicroRNAs); 0 (RNA, Small Interfering); 0 (Tumor Suppressor Protein p53); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); EC 3.4.22.- (Caspase 3); XV74C1N1AE (hydroquinone)
[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]:29339218
[Au] Autor:Liang J; Dou Y; Wu X; Li H; Wu J; Huang Q; Luo D; Yi T; Liu Y; Su Z; Chen J
[Ad] Endereço:Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
[Ti] Título:Prophylactic efficacy of patchoulene epoxide against ethanol-induced gastric ulcer in rats: Influence on oxidative stress, inflammation and apoptosis.
[So] Source:Chem Biol Interact;283:30-37, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Patchoulene epoxide (PAO), a tricyclic sesquiterpene isolated from the long-stored patchouli oil, has been demonstrated the anti-inflammatory activity in vivo based on our previous study. However, the gastric protective effect of PAO still remains unknown. Therefore, in the present study, ethanol-induced gastric ulcer model was carried out to evaluate the anti-ulcerogenic activity of PAO and to elucidate the potential mechanisms that involves. According to our results, macroscopic examination revealed that PAO could significantly reduce ethanol-induced gastric ulcer areas as compared with the vehicle group, which was also supported by the histological evaluation result. As for its potential mechanism, the anti-inflammatory activity of PAO contributed to gastric protection through reversing the imbalance between pro- and anti-inflammatory cytokines and modulating the expressions of NF-κB pathway-related proteins including p-IκBα, IκBα, p-p65 and p65. Besides, PAO was able to enhance the expressions of antioxidant enzymes including glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT), and down-regulate malonaldehyde (MDA), an indicator of lipid peroxidation. Furthermore, immunohistochemistry analysis exhibited potent anti-apoptosis effect of PAO, as evidence by down-regulating the protein expression of caspase-3, Fas and Fasl. Additionally, we also demonstrated that PAO could replenish PGE and NO mucosal defense. In conclusion, these findings suggested that PAO has gastric protective activity against ethanol and this might be related to its influence on inflammatory response, oxidative stress, apoptosis cascade and gastric mucosal defense.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Sesquiterpenos/farmacologia
Úlcera Gástrica/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Anti-Inflamatórios/uso terapêutico
Caspase 3/metabolismo
Catalase/metabolismo
Citocinas/análise
Citocinas/metabolismo
Regulação para Baixo/efeitos dos fármacos
Etanol/toxicidade
Inflamação/prevenção & controle
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Óleos Vegetais/química
Pogostemon/química
Pogostemon/metabolismo
Ratos
Ratos Sprague-Dawley
Sesquiterpenos/química
Sesquiterpenos/uso terapêutico
Estômago/patologia
Úlcera Gástrica/induzido quimicamente
Úlcera Gástrica/patologia
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Plant Oils); 0 (Sesquiterpenes); 3K9958V90M (Ethanol); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.22.- (Caspase 3)
[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:180118
[St] Status:MEDLINE


  8 / 27382 MEDLINE  
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[PMID]:29184399
[Au] Autor:Wu C; Xu J; Hao Y; Zhao Y; Qiu Y; Jiang J; Yu T; Ji P; Liu Y
[Ad] Endereço:Pharmacy School, Jinzhou Medical University, Jinzhou, China.
[Ti] Título:Application of a lipid-coated hollow calcium phosphate nanoparticle in synergistic co-delivery of doxorubicin and paclitaxel for the treatment of human lung cancer A549 cells.
[So] Source:Int J Nanomedicine;12:7979-7992, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:In this study, we developed a lipid-coated hollow calcium phosphate (LCP) nanoparticle for the combined application of two chemotherapeutic drugs to human lung cancer A549 cells. Hydrophilic doxorubicin (DOX) was incorporated into the hollow structure of hollow calcium phosphate (HCP), and a lipid bilayer containing hydrophobic paclitaxel (PTX) was subsequently coated on the surface of HCP. The study on combinational effects demonstrated that the combination of DOX and PTX at a mass ratio of 12:1 showed a synergistic effect against A549 cells. The particle size, zeta potential, and encapsulation efficiency were measured to obtain optimal values: particle size was 335.0 3.2 nm, zeta potential -41.1 mV, and encapsulation efficiency 80.40%±2.24%. An in vitro release study indicated that LCP produced a sustained drug release. A549 cells had a better uptake of LCP with good biocompatibility. Furthermore, in vitro cytotoxicity experiment, apoptosis analysis, in vivo anti-tumor efficacy and protein expression analysis of Bax, Bcl-2, and Caspase-3 demonstrated that the co-delivery system based on LCP had significant synergistic anti-tumor activity. All conclusions suggested that LCP is a promising platform for co-delivery of multiple anti-tumor drugs.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Sistemas de Liberação de Medicamentos/métodos
Nanopartículas/administração & dosagem
Nanopartículas/química
Fosfolipídeos/química
[Mh] Termos MeSH secundário: Células A549
Animais
Protocolos de Quimioterapia Combinada Antineoplásica/farmacocinética
Apoptose/efeitos dos fármacos
Fosfatos de Cálcio/química
Caspase 3/metabolismo
Preparações de Ação Retardada/administração & dosagem
Preparações de Ação Retardada/química
Doxorrubicina/administração & dosagem
Doxorrubicina/química
Seres Humanos
Camundongos Nus
Paclitaxel/administração & dosagem
Paclitaxel/química
Tamanho da Partícula
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Phosphates); 0 (Delayed-Action Preparations); 0 (Phospholipids); 80168379AG (Doxorubicin); 97Z1WI3NDX (calcium phosphate); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); P88XT4IS4D (Paclitaxel)
[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:171130
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S140957


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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]:28627259
[Au] Autor:Zhang X; Li D; Xue X; Zhang Y; Zhang J; Huang C; Guo Z; Tadesse N
[Ad] Endereço:a School of Pharmacy, Health Science Center , Xi'an Jiaotong University , Xi'an , P.R. China.
[Ti] Título:First total synthesis of a novel amide alkaloid derived from Aconitum taipeicum and its anticancer activity.
[So] Source:Nat Prod Res;32(2):128-132, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A concise total synthesis of a naturally occurring 3-isopropyl-tetrahydropyrrolo[1, 2-a]pyrimidine-2, 4(1H, 3H)-dione (ITPD) isolated from Aconitum taipeicum with a three-step approach was depicted in this study for the first time. Two key intermediates, diethyl isopropylmalonate (2) and pyrrolidin-2-amine (3), being synthsesised separately from initial diethyl malonate (4) and 3, 4-dihydro-2H-pyrrol-5-amine (5), were utilised to obtain the compound entitled ITPD. ITPD showed a promising anticancer activity in vitro on SMMC-7721 cell lines. Flow cytometry and cell cycle analysis revealed that ITPD could induce apoptosis and cell cycle arrest in S phase. The occurrence of apoptosis possibly attributed to the mechanism that ITPD could mediate the mitochondrial pathway through activating caspase-3/9 and increasing the ratio of Bax/Bcl-2 to finally trigger cell apoptosis and DNA damage. Collectively, the possibility to produce sufficient quantity of synthetic ITPD provided the base for further bio-evaluation in vivo and in vitro. The bioactive assay suggested that it may be a potential candidate for further chemical optimisation and use in cancer therapy.
[Mh] Termos MeSH primário: Aconitum/química
Alcaloides/síntese química
Antineoplásicos Fitogênicos/síntese química
[Mh] Termos MeSH secundário: Alcaloides/farmacologia
Amidas/síntese química
Amidas/farmacologia
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Dano ao DNA/efeitos dos fármacos
Seres Humanos
Mitocôndrias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Amides); 0 (Antineoplastic Agents, Phytogenic); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1340283



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