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[PMID]:29175698
[Au] Autor:Santos Á; Soares JX; Cravo S; Tiritan ME; Reis S; Afonso C; Fernandes C; Pinto MMM
[Ad] Endereço:Laboratório de Química Orgânica e Farmacêutica, Departamento de Ciências Químicas, Faculdade de Farmácia, Universidade do Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal.
[Ti] Título:Lipophilicity assessement in drug discovery: Experimental and theoretical methods applied to xanthone derivatives.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1072:182-192, 2018 Jan 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:For the last several years, searching of new xanthone derivatives (XDs) with potential pharmacological activities has remained one of the main areas of interest of our group. The optimization of biological activity and drug-like properties of hits and leads is crucial at early stage of the drug discovery pipeline. Lipophilicity is one of the most important drug-like properties having a great impact in both pharmacokinetics and pharmacodynamics processes. In this work, we describe the lipophilicity of a small library of bioactive XDs, previously synthesized by our group, using different methods: computational, vortex-assisted liquid-liquid microextraction coupled with high-performance liquid chromatography (VALLME-HPLC), reversed-phase high-performance thin layer chromatography (RP-HPTLC), reversed-phase high-performance liquid chromatography (RP-HPLC), and biomembrane model by the partition between micelles and aqueous phase. The different results obtained by the used methods were compared and discussed. The methodologies and data gathered in this study will expand the investigation of lipophilicity of XDs, an important class of compounds in medicinal chemistry.
[Mh] Termos MeSH primário: Descoberta de Drogas/métodos
Xantonas/análise
Xantonas/química
[Mh] Termos MeSH secundário: Cromatografia Líquida de Alta Pressão/métodos
Cromatografia de Fase Reversa/métodos
Interações Hidrofóbicas e Hidrofílicas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Xanthones)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  2 / 2609 MEDLINE  
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[PMID]:28464819
[Au] Autor:Imran M; Arshad MS; Butt MS; Kwon JH; Arshad MU; Sultan MT
[Ad] Endereço:Department of Diet and Nutritional Sciences, Imperial College of Business Studies, Lahore, Pakistan.
[Ti] Título:Mangiferin: a natural miracle bioactive compound against lifestyle related disorders.
[So] Source:Lipids Health Dis;16(1):84, 2017 May 02.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The current review article is an attempt to explain the therapeutic potential of mangiferin, a bioactive compound of the mango, against lifestyle-related disorders. Mangiferin (2-ß-D-glucopyranosyl-1,3,6,7-tetrahydroxy-9H-xanthen-9-one) can be isolated from higher plants as well as the mango fruit and their byproducts (i.e. peel, seed, and kernel). It possesses several health endorsing properties such as antioxidant, antimicrobial, antidiabetic, antiallergic, anticancer, hypocholesterolemic, and immunomodulatory. It suppresses the activation of peroxisome proliferator activated receptor isoforms by changing the transcription process. Mangiferin protects against different human cancers, including lung, colon, breast, and neuronal cancers, through the suppression of tumor necrosis factor α expression, inducible nitric oxide synthase potential, and proliferation and induction of apoptosis. It also protects against neural and breast cancers by suppressing the expression of matrix metalloproteinase (MMP)-9 and MMP-7 and inhibiting enzymatic activity, metastatic potential, and activation of the ß-catenin pathway. It has the capacity to block lipid peroxidation, in order to provide a shielding effect against physiological threats. Additionally, mangiferin enhances the capacity of the monocyte-macrophage system and possesses antibacterial activity against gram-positive and gram-negative bacteria. This review summarizes the literature pertaining to mangiferin and its associated health claims.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Antineoplásicos Fitogênicos/uso terapêutico
Antioxidantes/uso terapêutico
Hipoglicemiantes/uso terapêutico
Nootrópicos/uso terapêutico
Xantonas/uso terapêutico
[Mh] Termos MeSH secundário: Anti-Inflamatórios/química
Anti-Inflamatórios/isolamento & purificação
Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/isolamento & purificação
Antioxidantes/química
Antioxidantes/isolamento & purificação
Doenças Cardiovasculares/tratamento farmacológico
Doenças Cardiovasculares/patologia
Disfunção Cognitiva/tratamento farmacológico
Disfunção Cognitiva/patologia
Diabetes Mellitus Tipo 2/tratamento farmacológico
Diabetes Mellitus Tipo 2/patologia
Seres Humanos
Hiperlipidemias/tratamento farmacológico
Hiperlipidemias/patologia
Hipoglicemiantes/química
Hipoglicemiantes/isolamento & purificação
Mangifera/química
Neoplasias/tratamento farmacológico
Neoplasias/patologia
Neuralgia/tratamento farmacológico
Neuralgia/patologia
Nootrópicos/química
Nootrópicos/isolamento & purificação
Estresse Oxidativo/efeitos dos fármacos
Xantonas/química
Xantonas/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antineoplastic Agents, Phytogenic); 0 (Antioxidants); 0 (Hypoglycemic Agents); 0 (Nootropic Agents); 0 (Xanthones); 1M84LD0UMD (mangiferin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-017-0449-y


  3 / 2609 MEDLINE  
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[PMID]:29317203
[Au] Autor:Liu T; Duan W; Nizigiyimana P; Gao L; Liao Z; Xu B; Liu L; Lei M
[Ad] Endereço:Department of Endocrinology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China; Department of Endocrinology, Haikou People's Hospital, Haikou, Hainan, 570208, China.
[Ti] Título:Alpha-mangostin attenuates diabetic nephropathy in association with suppression of acid sphingomyelianse and endoplasmic reticulum stress.
[So] Source:Biochem Biophys Res Commun;496(2):394-400, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Diabetic nephropathy is a common complication of diabetes, but there are currently few treatment options. The aim of this study was to gain insight into the effect of alpha-mangostin on diabetic nephropathy and possible related mechanisms. METHODS: Goto-Kakizaki rats were used as a diabetic model and received alpha-mangostin or desipramine treatment with normal saline as a control. Ten age-matched Sprague Dawley rats were used as normal controls and treated with normal saline. At week 12, blood glucose, albuminuria, apoptosis and renal pathologic changes were assessed. Protein levels for acid sphingomyelinase, glucose-regulated protein 78, phosphorylated PKR-like ER-resident kinase, activated transcription factor 4, CCAAT/enhancer-binding protein, homologous protein), and cleaved-caspase12 were measured. RESULTS: The level of acid sphingomyelinase was significantly increased, and ER stress was activated in diabetic rat kidneys when compared to the control animals. When acid sphingomyelinase was inhibited by alpha-mangostin, the expression of ER stress-related proteins was down-regulated in association with decreased levels of diabetic kidney injury. CONCLUSIONS: Alpha-mangostin, an acid sphingomyelinase inhibitor plays a protective role in diabetic neuropathy by relieving ER stress induced-renal cell apoptosis.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Nefropatias Diabéticas/tratamento farmacológico
Inibidores Enzimáticos/farmacologia
Substâncias Protetoras/farmacologia
Esfingomielina Fosfodiesterase/antagonistas & inibidores
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Fator 4 Ativador da Transcrição/metabolismo
Albuminúria/genética
Albuminúria/metabolismo
Albuminúria/patologia
Albuminúria/prevenção & controle
Animais
Apoptose/efeitos dos fármacos
Glicemia/metabolismo
Caspase 12/genética
Caspase 12/metabolismo
Desipramina/farmacologia
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/patologia
Nefropatias Diabéticas/induzido quimicamente
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/patologia
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Regulação da Expressão Gênica
Proteínas de Choque Térmico/genética
Proteínas de Choque Térmico/metabolismo
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Masculino
Ratos
Ratos Sprague-Dawley
Esfingomielina Fosfodiesterase/genética
Esfingomielina Fosfodiesterase/metabolismo
Estreptozocina
eIF-2 Quinase/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atf4 protein, rat); 0 (Blood Glucose); 0 (Enzyme Inhibitors); 0 (Heat-Shock Proteins); 0 (Hspa5 protein, rat); 0 (Protective Agents); 0 (Xanthones); 145891-90-3 (Activating Transcription Factor 4); 5W494URQ81 (Streptozocin); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.4.- (acid sphingomyelinase-1); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase); EC 3.4.22.- (Casp12 protein, rat); EC 3.4.22.- (Caspase 12); TG537D343B (Desipramine); U6RIV93RU1 (mangostin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


  4 / 2609 MEDLINE  
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[PMID]:29223569
[Au] Autor:Singh AK; Raj V; Keshari AK; Rai A; Kumar P; Rawat A; Maity B; Kumar D; Prakash A; De A; Samanta A; Bhattacharya B; Saha S
[Ad] Endereço:Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, Uttar Pradesh, India.
[Ti] Título:Isolated mangiferin and naringenin exert antidiabetic effect via PPAR /GLUT4 dual agonistic action with strong metabolic regulation.
[So] Source:Chem Biol Interact;280:33-44, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In this study, we isolated two compounds from the leaves of Salacia oblonga (SA1, mangiferin and SA2, naringenin), and their structures were confirmed by infrared spectroscopy, nuclear magnetic resonance (NMR) spectroscopy, and mass spectrometry. SA1 and SA2 were orally administered to streptozotocin-induced diabetic rats at 50 and 100 mg/kg daily for 15 days. Blood glucose level, serum lipid profile, oxidative stress parameters, histopathology, docking, molecular parameters, and NMR-based metabolic perturbation studies were performed to investigate the pharmacological activities of SA1 and SA2. Results suggested that both compounds reduced blood glucose level, restored body weight, and normalized lipid concentrations in the serum and oxidative stress biomarkers in the liver and pancreas. In addition, the docking study on several diabetes-associated targets revealed that both compounds had a strong binding affinity towards peroxisome proliferator-activated receptor gamma (PPAR ) and glucose transporter type 4 (GLUT4). Further real-time reverse transcription polymerase chain reaction and western blot analyses were performed to confirm the gene and protein expression levels of PPAR and GLUT4 in the pancreatic tissues. Data obtained from the molecular studies showed that both compounds exhibited antidiabetic effects through dual activation of PPAR /GLUT4 signaling pathways. Finally, the NMR-based metabolic studies showed that both compounds normalized the diabetogenic metabolites in the serum. Altogether, we concluded that SA1 and SA2 might be potential antidiabetic lead compounds for future drug development.
[Mh] Termos MeSH primário: Flavanonas/farmacologia
Transportador de Glucose Tipo 4/metabolismo
Hipoglicemiantes/farmacologia
PPAR gama/metabolismo
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/análise
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/tratamento farmacológico
Flavanonas/isolamento & purificação
Flavanonas/uso terapêutico
Transportador de Glucose Tipo 4/agonistas
Transportador de Glucose Tipo 4/genética
Glicogênio/metabolismo
Hipoglicemiantes/isolamento & purificação
Hipoglicemiantes/uso terapêutico
Insulina/sangue
Lipídeos/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Simulação de Acoplamento Molecular
Estresse Oxidativo/efeitos dos fármacos
PPAR gama/agonistas
PPAR gama/genética
Pâncreas/efeitos dos fármacos
Pâncreas/metabolismo
Pâncreas/patologia
Estrutura Terciária de Proteína
Ratos
Salacia/química
Salacia/metabolismo
Transdução de Sinais/efeitos dos fármacos
Estreptozocina/toxicidade
Xantonas/isolamento & purificação
Xantonas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Flavanones); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Lipids); 0 (PPAR gamma); 0 (Xanthones); 1M84LD0UMD (mangiferin); 5W494URQ81 (Streptozocin); 9005-79-2 (Glycogen); HN5425SBF2 (naringenin)
[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:171211
[St] Status:MEDLINE


  5 / 2609 MEDLINE  
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[PMID]:29172759
[Au] Autor:Wang S; Shao M; Zhong Z; Wang A; Cao J; Lu Y; Wang Y; Zhang J
[Ad] Endereço:a State Key Laboratory of Quality Research in Chinese Medicine , Institute of Chinese Medical Sciences, University of Macau , Macau , China.
[Ti] Título:Co-delivery of gambogic acid and TRAIL plasmid by hyaluronic acid grafted PEI-PLGA nanoparticles for the treatment of triple negative breast cancer.
[So] Source:Drug Deliv;24(1):1791-1800, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based combination therapy and gene therapy are new strategies to potentially overcome the limitations of TRAIL, however, the lack of efficient and low toxic vectors remains the major obstacle. In this study, we developed a hyaluronic acid (HA)-decorated polyethylenimine-poly(d,l-lactide-co-glycolide) (PEI-PLGA) nanoparticle (NP) system for targeted co-delivery of TRAIL plasmid (pTRAIL) and gambogic acid (GA) in triple-negative breast cancer (TNBC) therapy. GA was encapsulated into the core of the PEI-PLGA NPs while pTRAIL was adsorbed onto the positive NP surface via charge adsorption. The coating of HA on PEI-PLGA NPs functions as a targeting ligand by binding to CD44 receptor of TNBC cells and a shell to neutralize the excess positive charge of inner NPs. The resultant pTRAIL and GA co-loaded HA-coated PEI-PLGA NPs exhibited spherical shape (121.5 nm) and could promote the internalization of loaded cargoes into TNBC cells through the CD44-dependent endocytic pathway. The dual drug-loaded NPs significantly augmented apoptotic cell death in vitro and inhibited TNBC tumor growth in vivo. This multifunctional NP system efficiently co-delivered GA and pTRAIL, thus representing a promising strategy to treat TNBC and bringing forth a platform strategy for co-delivery of therapeutic DNA and chemotherapeutic agents in combinatorial TNBC therapy.
[Mh] Termos MeSH primário: Ácido Hialurônico/administração & dosagem
Ácido Láctico/administração & dosagem
Nanopartículas/administração & dosagem
Plasmídeos/administração & dosagem
Polietilenoimina/administração & dosagem
Ácido Poliglicólico/administração & dosagem
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Xantonas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Portadores de Fármacos/administração & dosagem
Seres Humanos
Receptores de Hialuronatos/metabolismo
Células MCF-7
Camundongos
Neoplasias de Mama Triplo Negativas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Carriers); 0 (Hyaluronan Receptors); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Xanthones); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 8N585K83U2 (gambogic acid); 9002-98-6 (Polyethyleneimine); 9004-61-9 (Hyaluronic 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:171128
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1406558


  6 / 2609 MEDLINE  
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[PMID]:29190630
[Au] Autor:Chen CM; Hsieh SC; Lin CL; Lin YS; Tsai JP; Hsieh YH
[Ad] Endereço:Division of Neurosurgery, Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan.
[Ti] Título:Alpha-Mangostin Suppresses the Metastasis of Human Renal Carcinoma Cells by Targeting MEK/ERK Expression and MMP-9 Transcription Activity.
[So] Source:Cell Physiol Biochem;44(4):1460-1470, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: α-mangostin has anti-carcinogenic effects against several cancers. We investigated the molecular mechanism of this compound on the metastasis of human renal carcinoma cells. METHODS: Cell viability was measured using the MTT assay, and cell cycle distribution using flow cytometry. A Matrigel-based assay was used to measure in vitro cell migration and invasion. MAPK-related proteins and matrix metalloproteinase (MMP)-9 and MMP-2 expression were measured by western blotting, and MMP2/-9 activities were determined by gelatin zymography. RT-qPCR and a luciferase assay were used to examine the transcriptional activity of MMP-9. RESULTS: α-mangostin inhibited the migration and invasion of RCC cells in a dose-dependent manner, but had no evident cytotoxic effects. Treatment of 786-O cells with α-mangostin inhibited activation of MEK and ERK. Treatment with a specific MEK inhibitor (U0126) enhanced the inhibitory effects of α-mangostin on cell migration and invasion, and the phosphorylation of ERK and MEK. Moreover, α-mangostin inhibited the expression of the MMP-9 mRNA levels as well as the activity of MMP-9 promoter, and these suppressive effects were further enhanced by U0126. CONCLUSIONS: Our results suggest that α-mangostin suppresses cell migration and invasion via MEK/ERK/MMP9 pathway, and might be a promising anti-metastatic agent against human renal cell carcinoma.
[Mh] Termos MeSH primário: Anticarcinógenos/toxicidade
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
MAP Quinase Quinase Quinases/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Xantonas/toxicidade
[Mh] Termos MeSH secundário: Anticarcinógenos/química
Butadienos/farmacologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Neoplasias Renais/metabolismo
Neoplasias Renais/patologia
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Nitrilos/farmacologia
Xantonas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Butadienes); 0 (Nitriles); 0 (U 0126); 0 (Xanthones); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); U6RIV93RU1 (mangostin)
[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:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000485582


  7 / 2609 MEDLINE  
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[PMID]:29186708
[Au] Autor:Zhao W; Peng F; Shu M; Liu H; Hou X; Wang X; Ye J; Zhao B; Wang K; Zhong C; Xue L; Gao M; Liu Y; Zhao S
[Ad] Endereço:Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
[Ti] Título:Isogambogenic Acid Inhibits the Growth of Glioma Through Activation of the AMPK-mTOR Pathway.
[So] Source:Cell Physiol Biochem;44(4):1381-1395, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Glioma is the most devastating cancer in the brain and has a poor prognosis in adults. Therefore, there is a critical need for novel therapeutic strategies for the management of glioma patients. Isogambogenic acid, an active compound extracted from the Chinese herb Garcinia hanburyi, induces autophagic cell death. METHODS: Cell viability was detected with MTT assays. Cell proliferation was assessed using the colony formation assay. Morphological changes associated with autophagy and apoptosis were tested by TEM and Hoechst staining, respectively. The apoptosis rate was measured by flow cytometry. Western blot, immunofluorescence and immunohistochemical analyses were used to detect protein expression. U87-derived xenografts were established for the examination of the effect of isogambogenic acid on glioma growth in vivo. RESULTS: Isogambogenic acid induced autophagic death in U87 and U251 cells, and blocking late-stage autophagy markedly enhanced the antiproliferative activities of isogambogenic acid. Moreover, we observed the activation of AMPK-mTOR signalling in isogambogenic acid-treated glioma cells. Furthermore, the activation of AMPK or the inhibition of mTOR augmented isogambogenic acid-induced autophagy. Inhibition of autophagy attenuated apoptosis in isogambogenic acid-treated glioma cells. Finally, isogambogenic acid inhibited the growth of U87 glioma in vivo. CONCLUSION: Isogambogenic acid inhibits the growth of glioma via activation of the AMPK-mTOR signalling pathway, which may provide evidence for future clinical applications in glioma therapy.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Antineoplásicos/toxicidade
Proliferação Celular/efeitos dos fármacos
Serina-Treonina Quinases TOR/metabolismo
Xantonas/toxicidade
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/farmacologia
Animais
Antineoplásicos/química
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Glioma/tratamento farmacológico
Glioma/patologia
Seres Humanos
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Transdução de Sinais/efeitos dos fármacos
Transplante Heterólogo
Xantonas/química
Xantonas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Xanthones); 0 (isogambogenic acid); 5142-23-4 (3-methyladenine); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.31 (AMP-Activated Protein Kinases); JAC85A2161 (Adenine)
[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:171130
[St] Status:MEDLINE
[do] DOI:10.1159/000485535


  8 / 2609 MEDLINE  
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[PMID]:29198894
[Au] Autor:Singla R; Gupta KB; Upadhyay S; Dhiman M; Jaitak V
[Ad] Endereço:Centre for Pharmaceutical Sciences and Natural Products, Central University of Punjab, Bathinda, India.
[Ti] Título:Design, synthesis and biological evaluation of novel indole-xanthendione hybrids as selective estrogen receptor modulators.
[So] Source:Bioorg Med Chem;26(1):266-277, 2018 01 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ground breaking clinical therapeutic advances in the treatment of breast cancer (BC) is the introduction of selective estrogen receptor modulators (SERMs). We have expeditiously designed and synthesized indole-xanthendione hybrids by coalescing the indole nucleus with xanthendione. All the compounds were first screened for anti-proliferative activity, cytotoxicity and ER-α binding affinity by utilizing ER-α dominant T47D BC cell lines, PBMCs and ER-α competitor assay kit. From this study, two representative compounds 6e and 6f showing most promising activity were advanced for gene expression studies for targeting ER-α. Cell imaging experiment undoubtedly indicate that both the compounds were able to cross cellular bio membrane and accumulate thus instigating cytotoxicity. RT-PCR and Western blotting experiments further strengthened that both compounds altered the expression of mRNA and receptor protein of ER-α, thereby forestalling downstream transactivation and signalling pathway in T47D cells line. Structural investigation from induced fit simulation study suggest that indole moiety of the compounds 6e and 6f helps in the anchoring of the xanthendione moiety in the hydrophobic region of the cavity thus enabling the compound to bind in antagonistic conformation similar to bazedoxifene by extensive hydrogen bonding and Van der Waals forces. All these finding collectively imply that compound 6e and 6f represents a novel potent ER-α antagonist and in the development of SERMs for the management of BC.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Desenho de Drogas
Moduladores de Receptor Estrogênico/farmacologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Indóis/farmacologia
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Moduladores de Receptor Estrogênico/síntese química
Moduladores de Receptor Estrogênico/química
Receptor alfa de Estrogênio/metabolismo
Seres Humanos
Indóis/química
Estrutura Molecular
Relação Estrutura-Atividade
Xantonas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Estrogen Receptor Modulators); 0 (Estrogen Receptor alpha); 0 (Indoles); 0 (Xanthones); 0 (estrogen receptor alpha, human); 8724FJW4M5 (indole)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180106
[Lr] Data última revisão:
180106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


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[PMID]:29232404
[Au] Autor:Zheng XY; Zhao X; Yang YF; Jiang HJ; Li W; Sun Y; Pu XP
[Ad] Endereço:National Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing, P. R. China.
[Ti] Título:Antioxidant, antiapoptotic and amino acid balance regulating activities of 1,7-dihydroxy-3,4,8-trimethoxyxanthone against dimethylnitrosamine-induced liver fibrosis.
[So] Source:PLoS One;12(12):e0189344, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Liver fibrosis represents the consequences of a sustained wound healing response to chronic liver injury which could be caused by viral, autoimmune, drugs, and so on. Unfortunately, there was no effective therapy available for liver fibrosis in clinic. In this study, we identified the anti-fibrotic effects of 1,7-dihydroxy-3,4,8-trimethoxyxanthone (ZYC-1) on the dimethylnitrosamine (DMN)-induced rat model. ZYC-1 was isolated from Swertia punicea Hemsl and was administrated to DMN-induced rat model. ZYC decreased the hyaluronic acid (HA), type IV collagen (CIV) and hydroxyproline (Hyp) levels and inhibited the expression of α smooth muscle actin (α-SMA) and transforming growth factor beta 1 (TGF-1ß). The anti-fibrotic effect of ZYC-1 was also confirmed by Sirius Red staining. Finally, we identified 42 differentially expressed proteins by using proteomics analysis after ZYC-1 treatment, of which 17 were up-regulated and 25 were down-regulated. These Most of the 42 proteins are involved in the oxidative stress pathway, the mitochondrial-mediated apoptotic pathway and the amino acid metabolism pathway. Our study presented the first elucidated mechanisms of xanthone on liver fibrosis in vivo. This study pointed out that ZYC-1 may be used as a lead compound for hepatofibrosis treatment.
[Mh] Termos MeSH primário: Aminoácidos/análise
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Dimetilnitrosamina/toxicidade
Cirrose Hepática/prevenção & controle
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Cirrose Hepática/induzido quimicamente
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,7-dihydroxy-3,4,8-trimethoxyxanthone); 0 (Amino Acids); 0 (Antioxidants); 0 (Xanthones); M43H21IO8R (Dimethylnitrosamine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189344


  10 / 2609 MEDLINE  
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[PMID]:29110583
[Au] Autor:Omer FAA; Hashim NBM; Ibrahim MY; Dehghan F; Yahayu M; Karimian H; Salim LZA; Mohan S
[Ad] Endereço:1 Department of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
[Ti] Título:Beta-mangostin from Cratoxylum arborescens activates the intrinsic apoptosis pathway through reactive oxygen species with downregulation of the HSP70 gene in the HL60 cells associated with a G /G cell-cycle arrest.
[So] Source:Tumour Biol;39(11):1010428317731451, 2017 Nov.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Xanthones are phytochemical compounds found in a number of fruits and vegetables. Characteristically, they are noted to be made of diverse properties based on their biological, biochemical, and pharmacological actions. Accordingly, the apoptosis mechanisms induced by beta-mangostin, a xanthone compound isolated from Cratoxylum arborescens in the human promyelocytic leukemia cell line (HL60) in vitro, were examined in this study. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was done to estimate the cytotoxicity effect of ß-mangostin on the HL60 cell line. Acridine orange/propidium iodide and Hoechst 33342 dyes and Annexin V tests were conducted to detect the apoptosis features. Caspase-3 and caspase-9 activities; reactive oxygen species; real-time polymerase chain reaction for Bcl-2, Bax, caspase-3, and caspase-9 Hsp70 genes; and western blot for p53, cytochrome c, and pro- and cleavage-caspase-3 and caspase-9 were assessed to examine the apoptosis mechanism. Cell-cycle analysis conducted revealed that ß-mangostin inhibited the growth of HL60 at 58 µM in 24 h. The administration of ß-mangostin with HL60 caused cell morphological changes related to apoptosis which increased the number of early and late apoptotic cells. The ß-mangostin-catalyzed apoptosis action through caspase-3, caspase-7, and caspase-9 activation overproduced reactive oxygen species which downregulated the expression of antiapoptotic genes Bcl-2 and HSP70. Conversely, the expression of the apoptotic genes Bax, caspase-3, and caspase-9 were upregulated. Meanwhile, at the protein level, ß-mangostin activated the formation of cleaved caspase-3 and caspase-9 and also upregulated the p53. ß-mangostin arrested the cell cycle at the G /G phase. Overall, the results for ß-mangostin showed an antiproliferative effect in HL60 via stopping the cell cycle at the G /G phase and prompted the intrinsic apoptosis pathway.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Proteínas de Choque Térmico HSP70/efeitos dos fármacos
Leucemia Promielocítica Aguda
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Clusiaceae
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células HL-60
Proteínas de Choque Térmico HSP70/biossíntese
Seres Humanos
Extratos Vegetais/farmacologia
Espécies Reativas de Oxigênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (HSP70 Heat-Shock Proteins); 0 (Plant Extracts); 0 (Reactive Oxygen Species); 0 (Xanthones); U6RIV93RU1 (mangostin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171108
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317731451



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