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Safrole Oxide Inhibits Angiogenesis by Inducing ApoptosisZhao, Jing, Miao, Junying, Zhao, Baoxiang, Zhang, Shangli, Yin, Deling 01 June 2005 (has links)
Our previous studies indicate that 3, 4-(methylenedioxy)-1-(2′, 3′-epoxypropyl)-benzene (safrole oxide), a newly synthesized compound, induces apoptosis in vascular endothelial cells (VECs) and A549 lung cancer cells. To our knowledge, the inhibition of angiogenesis by safrole oxide has not been reported yet. We report here that cultured rat aorta treated with safrole oxide exhibited a significant microvessel reduction as determined by counting the number of microvessels in a phase contrast microscope. There were more microvessels formed in the presence of A549 lung cancer cells in rat aorta model, while a dramatic inhibition of angiogenesis was obtained by adding 220-450 μmol l- 1 of safrole oxide to the growth medium (P <. 01). The culture of rat aorta treated with safrole oxide produced only some abortive endothelial cells but not microvessels. Furthermore, safrole oxide induced antiangiogenic effect in the chorioallantoic membranes (CAM) as a dose dependent manner. Eggs treated with 2-11 μmol 100 μl- 1 per egg of the safrole oxide for 48 h exhibited a significant reduction in blood vessel area of the CAM, a process likely mediated by apoptosis as demonstrated by DNA fragmentation. Our results suggest that safrole oxide has antiangiogenic activity and this effect might occur by induction of cellular apoptosis.
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Safrole Oxide Induced Human Umbilical Vein Vascular Endothelial Cell Differentiation Into Neuron-Like Cells by Depressing the Reactive Oxygen Species Level at the Low ConcentrationSu, Le, Zhao, Jing, Zhao, Bao Xiang, Miao, Jun Ying, Yin, De Ling, Zhang, Shang Li 01 February 2006 (has links)
Previously, we found that 5-25 μg/ml safrole oxide could inhibit apoptosis and dramatically make a morphological change in human umbilical vein vascular endothelial cells (HUVECs). But the possible mechanism by which safrole oxide function is unknown. To answer this question, in this study, we first investigated the effects of it on the activity of nitric oxide synthetase (NOS), the expressions of Fas and integrin β4, which play important roles in HUVEC growth and apoptosis, respectively. The results showed that, at the low concentration (10 μg/ml), safrole oxide had no effects on NOS activity and the expressions of Fas and integrin β4. Then, we investigated whether HUVECs underwent differentiation. We examined the expressions of neuron-specific enolase (NSE) and neurofilament-L (NF-L). Furthermore, we analyzed the changes of intracellular reactive oxygen species (ROS). After 10 h of treatment with 10 μg/ml safrole oxide, some HUVECs became neuron-like cells in morphology, and intensively displayed positive NSE and NF-L. Simultaneously, ROS levels dramatically decreased during HUVECs differentiation towards neuron-like cells. At the low concentration, safrole oxide induced HUVECs differentiation into neuron-like cells. Furthermore, our data suggested that safrole oxide might perform this function by depressing intracellular ROS levels instead of by affecting cell growth or apoptosis signal pathways.
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Safrole Oxide Induces Apoptosis by Activating Caspase-3, -8, and -9 in a549 Human Lung Cancer CellsDu, Ai, Zhao, Bao Xiang, Yin, De Ling, Zhang, Shang Li, Miao, Jun Ying 01 January 2006 (has links)
Previously we found that 3,4-(methylenedioxy)-1-(2′,3′- epoxypropyl)-benzene (safrole oxide) induced a typical apoptosis in A549 human lung cancer cells. In this study, we further investigated which caspases were activated by safrole oxide during the apoptosis. The data showed that the activity of caspase-3, -8, and -9 was significantly enhanced by the compound, which suggested that safrole oxide might be used as a caspase promoter to initiate lung cancer cell apoptosis.
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Síntese, comprovação estrutural e atividade antitumoral e antiparasitária de novos derivados benzodioxolicos / Síntese , caracterização estrutural e avaliação da atividade antitumoral e antiparasitária de novos derivados benzodioxolicosSILVA, Willams Leal 04 August 2016 (has links)
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Previous issue date: 2016-08-04 / FACEPE / O câncer destaca-se como um importante problema de saúde pública, além de configurar uma
das principais causas de morte no mundo. Considerando que em 2012 houve cerca de 8,2
milhões de mortes. Este trabalho teve como objetivo a obtenção de novos derivados benzo1,3-dioxol
(NW), por estratégia de hibridação molecular a fim de reunir características
estruturais em uma única estrutura com propriedades farmacológicas mista, dual ou dupla. A
síntese consiste na reação em duas rotas paralelas partindo dos aldeídos benzo[d][1,3]dioxol4-carbaldeído
e benzo[d][1,3]dioxol-5-carbaldeído, seguida de reações de condensação com
tiossemicarbazidas para obtenção de tiossemicarbazonas que podem ser conduzidas a uma
ciclização com ácido monocloroácetico formando o anel 4-tiazolidina. Todos os compostos
tiveram suas estruturas comprovadas por RMN1H, RMN 13C, COSY, IV e pirólise acoplado a
espectrometria de massas. Os compostos benzodioxois (NW) obtidos foram testados a fim de
avaliar a atividade antiproliferativa in vitro utilizando-se o ensaio da sulforrodamina B (SBR)
para avaliação do crescimento celular frente várias linhagens tumorais. Para o teste
antitumoral realizado os resultados obtidos mostram um derivado promissor NW-03 com GI50
estabelecidas entre 2,9 a 14,4 μM, quando comparado ao controle positivo utilizado. Diante
dos resultados obtidos os derivados foram classificados como ativos e mostraram um perfil
citostático. Além disso, os resultados obtidos corroboram para uma associação de núcleos
viáveis por meio da hibridação molecular entre o benzo-1,3-benzodioxol e tiossemicarbazona
levando a resultados promissores. Posteriormente os compostos foram submetidos a ensaios
de citoxicidade e avaliação antiparasitária onde foi possível eleger os compostos promissores
NW-03, NW-06 e NW-11 com baixa toxicidade para esplenócitos e atividade antiparasitária.
Em relação à atividade tripanocida, o composto NW-13 (1-naftil) exibiu elevados níveis de
atividade contra epimastigota e tripomastigota (IC50 = 1,48 e 3,89 µM, respectivamente). Com
o estudo de docking foi possível estabelecer correlação do encaixe de compostos NW-02 E
NW-09 com o alvo cruzaína através de interações. O composto NW-03 foi avaliado como
possível inibidor de tirosinase através de experimento de titulação por técnica de
espectroscopia de ressonância magnética nuclear e espectrofotometria. / The cancer stands out as a major public health problem, and configure one of the leading
causes of death worldwide. Whereas in 2012 there were about 8.2 million deaths. This study
aimed to obtain new derivatives benzo-1,3-dioxole (NW), by molecular hybridization strategy
to gather structural features in a single structure with mixed pharmacological properties, dual
or double. The synthesis consists of two parallel routes reaction starting from the aldehydes
benzo [d] [1,3] dioxol-4-carbaldehyde and benzo [d] [1,3] dioxol-5-carbaldehyde, followed by
condensation reactions to tiossemicarbazidas obtaining thiosemicarbazone that can be
conducted with a cyclized with monochloroacetic acid to form the 4-thiazolidine ring. All
compounds had their structures evidenced by 1 H NMR, 13C NMR, COSY, IV and coupled
pyrolysis mass spectrometry. Benzodioxoles The compounds (NW) have been tested in order
to assess the antiproliferative activity in vitro using the sulforhodamine B assay (SBR) for
evaluation of cell growth across various tumor cell lines. For antitumor test performed the
results obtained show a promising derived NW-03 GI50 established between 2.9 to 14.4 uM
when compared to the positive control used. Results obtained derivatives were classified as
active and showed a cytostatic profile. Moreover, the results support an association of viable
nuclei by means of molecular hybridization between the benzo-1,3-benzodioxole
thiosemicarbazone leading to promising results. Later the compounds were subjected to
cytotoxicity testing and antiparasitic assessment where it was possible to elect the promising
compounds NW-03, NW 06 and NW-11 with low toxicity to splenocytes and antiparasitic
activity. Regarding trypanocidal activity, NW-13 compound (1-naphthyl) exhibited high
levels of activity against epimastigote and trypomastigote (IC50 = 1.48 and 3.89 uM,
respectively). With the docking study was possible to establish compounds fitting correlation
NW-02 and NW-09 with the target cruzain through interactions. NW-03 The compound was
evaluated as a possible inhibitor of tyrosinase by titration experiment for technical nuclear
magnetic resonance spectroscopy, and spectrophotometry.
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Safrole Oxide Induces Apoptosis by up-Regulating Fas and FasL Instead of Integrin β4 in A549 Human Lung Cancer CellsDu, Ai, Zhao, Bao Xiang, Miao, Jun Ying, Yin, De Ling, Zhang, Shang Li 01 April 2006 (has links)
Previously, we found that 3,4-(methylenedioxy)-1-(2′,3′- epoxypropyl)-benzene (safrole oxide) induced a typical apoptosis in A549 human lung cancer cells by activating caspase-3, -8, and -9. In this study, we further investigated which upstream pathways were activated by safrole oxide during the apoptosis. Immunofluorescence assay combined with laser scanning confocal microscopy revealed that both Fas and Fas ligand (FasL) were up-regulated by the small molecule. In addition, Fas protein distribution was altered, showing a clustering distribution instead of a homogeneous one. Subsequently, Western blot analysis confirmed the up-regulations of Fas and its membrane-binding form of FasL (m-FasL), as well as P53 protein. Conversely, safrole oxide hardly affected integrin β4 subunit expression or distribution, which was reflected from the data obtained by immunofluorescence assay combined with laser scanning confocal microscopy. The results suggested that Fas/FasL pathway might be involved in safrole oxide-induced apoptosis of A549 cells, while integrin β4 might be irrelevant to the apoptosis. Nevertheless, we first found the strong expression of integrin β4 in A549 cells. The study first suggested that safrole oxide might be used as a small molecular promoter of Fas/FasL pathway to elicit apoptosis in A549 cells, which would lay the foundation for us to insight into the new strategies for lung cancer therapy.
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Suppressing Akt Phosphorylation and Activating Fas by Safrole Oxide Inhibited Angiogenesis and Induced Vascular Endothelial Cell Apoptosis in the Presence of Fibroblast Growth Factor-2 and SerumZhao, Jing, Miao, Junying, Zhao, Baoxiang, Zhang, Shangli, Yin, Deling 22 May 2006 (has links)
At present, vascular endothelial cell (VEC) apoptosis induced by deprivation of fibroblast growth factor-2 (FGF-2) and serum has been well studied. But how to trigger VEC apoptosis in the presence of FGF-2 and serum is not well known. To address this question, in this study, the effects of safrole oxide on angiogenesis and VEC growth stimulated by FGF-2 were investigated. The results showed that safrole oxide inhibited angiogenesis and induced VEC apoptosis in the presence of FGF-2 and serum. To understand the possible mechanism of safrole oxide acting, we first examined the phosphorylation of Akt and the activity of nitric oxide synthase (NOS); secondly, we analyzed the expressions and distributions of Fas and P53; then we measured the activity of phosphatidylcholine specific phospholipase C (PC-PLC) in the VECs treated with and without safrole oxide. The results showed that this small molecule obviously suppressed Akt phosphorylation and the activity of NOS, and promoted the expressions of Fas and P53 markedly. Simultaneously, Fas protein clumped on cell membrane, instead of homogenously distributed. The activity of PC-PLC was not changed obviously. The data suggested that safrole oxide effectively inhibited angiogenesis and triggered VEC apoptosis in the presence of FGF-2 and serum, and it might perform its functions by suppressing Akt/NOS signal pathway, upregulating the expressions of Fas and P53 and modifying the distributing pattern of Fas in VEC. This finding provided a powerful chemical probe for promoting VEC apoptosis during angiogenesis stimulated by FGF-2.
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