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1.
Phytomedicine ; 101: 154116, 2022 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-35525235

RESUMO

BACKGROUND: Despite recent advances in the treatment of squamous cell skin cancer (SCSC), the disease persists, and treatment resistance develops. Thus, identifying new targets and developing new therapeutic approaches showing low vulnerability to drug resistance is highly needed. PURPOSE: This study aimed to reveal a novel targeted phytotherapeutic strategy for SCSC treatment alone or in combination with standard targeted anticancer molecules. STUDY DESIGN: A library of natural products was utilized to identify molecules that inhibit the growth of skin cancer cells. The anticancer potential of the selected compound was evaluated in human skin squamous carcinoma models, in vitro and in vivo. A comprehensive ingenuity pathway analysis (IPA) strategy and molecular biology technology was adopted to investigate the therapeutic mechanisms in human SCSC. METHODS: The Matrigel invasion chamber, foci formation and soft agar colony formation assays were employed to study the cells invasion and migration potential in vitro. In vivo antitumor effects were evaluated in DMBA/TPA-induced skin papilloma and A431 human skin squamous carcinoma xenograft tumor models. An integrative IPA was employed to identify mechanisms and protein targets in human SCSC.Compounds synergies were determined by the bliss model and evaluated using human SCSC cell lines and xenograft tumors. Histological staining, immunofluorescence imaging, real-time PCR, Western blots, and flow cytometric analyses were employed to analyze apoptosis and cell signaling mechanisms. RESULTS: We identified (+)-cyanidan-3-ol (CD-3) as a selective compound for inhibiting the growth of SCSC cell lines. CD-3 inhibited tumor growth and burden without apparent toxicity and prolonged the survival of tumor-bearing mice. CD-3 inhibitory effects on SCSC growth are mediated via cell cycle arrest and caspase-dependent apoptosis induction. Mechanistic studies showed that CD-3 activates PP2A via inhibiting CIP2A and produces tumor growth inhibitory effects via promoting dephosphorylation of oncogenic AKT/mTOR signaling proteins in SCSC cells and xenograft tumors in a PP2A dependent manner. Furthermore, the combination of CD-3 and mTOR inhibitors (mTORi) synergistically reduced oncogenic phenotypes. CONCLUSIONS: Our study suggests that PP2A activation is an effective strategy for SCSC treatment and the CD-3 and mTORi combination may serve as a promising treatment for SCSC.


Assuntos
Carcinoma de Células Escamosas , Neoplasias Cutâneas , Animais , Humanos , Camundongos , Apoptose , Autoantígenos/genética , Autoantígenos/metabolismo , Autoantígenos/farmacologia , Carcinoma de Células Escamosas/tratamento farmacológico , Linhagem Celular Tumoral , Células Epiteliais/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Proteínas de Membrana/metabolismo , Proteína Fosfatase 2/metabolismo , Proteína Fosfatase 2/farmacologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Neoplasias Cutâneas/tratamento farmacológico , Serina-Treonina Quinases TOR/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto
2.
Front Mol Biosci ; 8: 667947, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34212002

RESUMO

TSPO-associated protein 1 (TSPOAP1) is a cytoplasmic protein and is closely associated with its mitochondrial transmembrane protein partner translocator protein (TSPO). To decipher the canonical signalling pathways of TSPOAP1, its role in human diseases and disorders, and relationship with TSPO; expression analyses of TSPOAP1- and TSPO-associated human genes were performed by Qiagen Ingenuity Pathway Analysis (IPA). In the expression analysis, necroptosis and sirtuin signalling pathways, mitochondrial dysfunction, and inflammasome were the top canonical pathways for both TSPOAP1 and TSPO, confirming the close relationship between these two proteins. A distribution analysis of common proteins in all the canonical pathways predicted for TSPOAP1 revealed that tumor necrosis factor receptor 1 (TNFR1), vascular cell adhesion molecule 1 (VCAM1), cyclic AMP response element-binding protein 1 (CREB1), T-cell receptor (TCR), nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3), DNA-dependent protein kinase (DNA-PK or PRKDC), and mitochondrial permeability transition pore (mPTP) were the major interaction partners of TSPOAP1, highlighting the role of TSPOAP1 in inflammation, particularly neuroinflammation. An analysis of the overlap between TSPO and TSPOAP1 Homo sapiens genes and top-ranked canonical pathways indicated that TSPO and TSPOAP1 interact via voltage-dependent anion-selective channels (VDAC1/2/3). A heat map analysis indicated that TSPOAP1 has critical roles in inflammatory, neuroinflammatory, psychiatric, and metabolic diseases and disorders, and cancer. Taken together, this information improves our understanding of the mechanism of action and biological functions of TSPOAP1 as well as its relationship with TSPO; furthermore, these results could provide new directions for in-depth functional studies of TSPOAP1 aimed at unmasking its detailed functions.

3.
J Pharmacol Exp Ther ; 376(3): 358-373, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33468641

RESUMO

Blebbistatin, para-nitroblebbistatin (NBleb), and para-aminoblebbistatin (AmBleb) are highly useful tool compounds as they selectively inhibit the ATPase activity of myosin-2 family proteins. Despite the medical importance of the myosin-2 family as drug targets, chemical optimization has not yet provided a promising lead for drug development because previous structure-activity-relationship studies were limited to a single myosin-2 isoform. Here we evaluated the potential of blebbistatin scaffold for drug development and found that D-ring substitutions can fine-tune isoform specificity, absorption-distribution-metabolism-excretion, and toxicological properties. We defined the inhibitory properties of NBleb and AmBleb on seven different myosin-2 isoforms, which revealed an unexpected potential for isoform specific inhibition. We also found that NBleb metabolizes six times slower than blebbistatin and AmBleb in rats, whereas AmBleb metabolizes two times slower than blebbistatin and NBleb in human, and that AmBleb accumulates in muscle tissues. Moreover, mutagenicity was also greatly reduced in case of AmBleb. These results demonstrate that small substitutions have beneficial functional and pharmacological consequences, which highlight the potential of the blebbistatin scaffold for drug development targeting myosin-2 family proteins and delineate a route for defining the chemical properties of further derivatives to be developed. SIGNIFICANCE STATEMENT: Small substitutions on the blebbistatin scaffold have beneficial functional and pharmacological consequences, highlighting their potential in drug development targeting myosin-2 family proteins.


Assuntos
Absorção Fisico-Química , Descoberta de Drogas , Compostos Heterocíclicos de 4 ou mais Anéis/metabolismo , Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia , Miosinas/antagonistas & inibidores , Animais , Compostos Heterocíclicos de 4 ou mais Anéis/química , Compostos Heterocíclicos de 4 ou mais Anéis/toxicidade , Humanos , Simulação de Dinâmica Molecular , Miosinas/química , Conformação Proteica , Ratos , Distribuição Tecidual
4.
Nat Prod Res ; 35(21): 3939-3944, 2021 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32316769

RESUMO

A simple and economical method was developed for the extraction and isolation of pentacyclic triterpenoid lantadene A from the leaves of Lantana camara. The lantadene A displays significant anti-inflammatory and anticancer properties via the inhibition of IKK-mediated NF-κB protein. Therefore, the derivatives of lantadene A were synthesised to further optimise the pharmacophore for anti-inflammatory and anticancer activities. The synthesised compounds were docked into the active site of IKK to find the most potent inhibitor of IKK. Molecular docking studies revealed that 3ß,22ß-diisobutyl substituted lantadene derivative (10) binds to the IKK protein with the highest affinity. Furthermore, in the in silico ADMET studies, the lead IKK inhibitor (10) was found to be Ames non-toxic, non-carcinogen, and a weak inhibitor of hERG.[Figure: see text].


Assuntos
Lantana , Ácido Oleanólico , Triterpenos , Lantana/química , Simulação de Acoplamento Molecular , Ácido Oleanólico/análogos & derivados , Ácido Oleanólico/isolamento & purificação , Triterpenos/isolamento & purificação
5.
Cell ; 183(2): 335-346.e13, 2020 10 15.
Artigo em Inglês | MEDLINE | ID: mdl-33035452

RESUMO

Muscle spasticity after nervous system injuries and painful low back spasm affect more than 10% of global population. Current medications are of limited efficacy and cause neurological and cardiovascular side effects because they target upstream regulators of muscle contraction. Direct myosin inhibition could provide optimal muscle relaxation; however, targeting skeletal myosin is particularly challenging because of its similarity to the cardiac isoform. We identified a key residue difference between these myosin isoforms, located in the communication center of the functional regions, which allowed us to design a selective inhibitor, MPH-220. Mutagenic analysis and the atomic structure of MPH-220-bound skeletal muscle myosin confirmed the mechanism of specificity. Targeting skeletal muscle myosin by MPH-220 enabled muscle relaxation, in human and model systems, without cardiovascular side effects and improved spastic gait disorders after brain injury in a disease model. MPH-220 provides a potential nervous-system-independent option to treat spasticity and muscle stiffness.


Assuntos
Músculo Esquelético/metabolismo , Miosinas de Músculo Esquelético/efeitos dos fármacos , Miosinas de Músculo Esquelético/genética , Adulto , Animais , Miosinas Cardíacas/genética , Miosinas Cardíacas/metabolismo , Linhagem Celular , Sistemas de Liberação de Medicamentos , Feminino , Humanos , Masculino , Camundongos , Contração Muscular/fisiologia , Fibras Musculares Esqueléticas/fisiologia , Espasticidade Muscular/genética , Espasticidade Muscular/fisiopatologia , Músculo Esquelético/fisiologia , Miosinas/efeitos dos fármacos , Miosinas/genética , Miosinas/metabolismo , Isoformas de Proteínas , Ratos , Ratos Wistar , Miosinas de Músculo Esquelético/metabolismo
6.
Mini Rev Med Chem ; 16(15): 1201-1218, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27121716

RESUMO

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the widely used medications all over the world, indicated for pain, fever, and inflammation. It is now well established that inflammation and cancer are closely linked with each other. Inflammatory mediators, like cyclooxygenase (COX), vascular endothelial growth factor (VEGF), tumor growth factor (TGF), fibroblast growth factor (FGF), chemokines, and cytokines and related genes, such as inhibitor of nuclear factor-kappa B kinase (IKK) and nuclear factor-kappa B (NF-κB) have been shown to be up-regulated in various cancers. Till date, numerous anticancer agents of different classes have been discovered to treat and eradicate various forms of cancer; though, limitations like cytotoxicity to normal cells and acquired tumor resistance restrict the scope of present cancer therapeutics. NSAIDs have shown to decrease the incidence, recurrence, and proliferation of various cancers, viz. colon, breast, lung, and pancreatic, etc. Therefore, the developing agents, such as NO-and H<sub>2</sub>S-releasing NSAIDs, NSAID-metal complexes, natural product-NSAID conjugates, phospho-NSAIDs, and various other NSAIDs derivatives represent the next generation therapeutics to treat both inflammation and cancer.


Assuntos
Anti-Inflamatórios não Esteroides/química , Anti-Inflamatórios não Esteroides/farmacologia , Antineoplásicos/química , Antineoplásicos/farmacologia , Descoberta de Drogas , Inflamação/tratamento farmacológico , Neoplasias/tratamento farmacológico , Animais , Anti-Inflamatórios não Esteroides/uso terapêutico , Antineoplásicos/uso terapêutico , Descoberta de Drogas/métodos , Humanos , Inflamação/complicações , Inflamação/imunologia , NF-kappa B/imunologia , Neoplasias/complicações , Neoplasias/imunologia , Prostaglandina-Endoperóxido Sintases/imunologia , Fator A de Crescimento do Endotélio Vascular/imunologia
7.
Food Funct ; 5(12): 3197-207, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25310126

RESUMO

An emulsified gel of (+)-catechin was developed and evaluated topically against 7,12-dimethylbenz(a)anthracene-induced and 12-O-tetradecanoylphorbol-13-acetate-promoted (DMBA-induced and TPA-promoted) squamous cell carcinoma of the skin in BALB/c mice. The biological evaluation outcome indicated that the (+)-catechin emulsified gel increased the activity of oxidative stress biomarkers glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx), whereas it decreased the level of malondialdehyde (MDA). The mechanistic study showed that genes implicated in the inflammation and cancer, such as cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-κB), and inducible nitric-oxide synthase (iNOS), were down-regulated by (+)-catechin emulsified gel while inhibiting an inflammatory mediator prostaglandin E2 (PGE2). The (+)-catechin emulsified gel further suppressed the activity of pro-inflammatory cytokines, viz. tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), and interleukin-6 (IL-6). The in vitro permeation study revealed that release of (+)-catechin from an emulsified gel base reached a steady state after 6 h, while pH of the entire emulsified gel was found to be between 6.2 and 6.5 that falls well within the normal pH range of the skin.


Assuntos
Acacia/química , Antioxidantes/metabolismo , Carcinoma de Células Escamosas/prevenção & controle , Catequina/administração & dosagem , Mediadores da Inflamação/metabolismo , Extratos Vegetais/administração & dosagem , Neoplasias Cutâneas/prevenção & controle , 9,10-Dimetil-1,2-benzantraceno/toxicidade , Administração Tópica , Animais , Biomarcadores/metabolismo , Carcinoma de Células Escamosas/induzido quimicamente , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Catequina/química , Dinoprostona/genética , Dinoprostona/metabolismo , Avaliação Pré-Clínica de Medicamentos , Emulsões/administração & dosagem , Humanos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo II/metabolismo , Extratos Vegetais/química , Neoplasias Cutâneas/induzido quimicamente , Neoplasias Cutâneas/genética , Neoplasias Cutâneas/metabolismo , Acetato de Tetradecanoilforbol/toxicidade , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
8.
Bioorg Med Chem Lett ; 24(16): 3814-8, 2014 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-25027934

RESUMO

The new series of pentacyclic triterpenoids reduced lantadene A (3), B (4), and 22ß-hydroxy-3-oxo-olean-12-en-28-oic acid (5) analogs were synthesized and tested in vitro for their NF-κB and IKKß inhibitory potencies and cytotoxicity against A549 lung cancer cells. The lead analog (11) showed sub-micromolar activity against TNF-α induced activation of NF-κB and exhibited inhibition of IKKß in a single-digit micromolar dose. At the same time, 11 showed promising cytotoxicity against A549 lung cancer cells with IC50 of 0.98 µM. The Western blot analysis further showed that the suppression of NF-κB activity by the lead analog 11 was due to the inhibition of IκBα degradation, a natural inhibitor of NF-κB. The physicochemical evaluation demonstrated that the lead analog 11 was stable in the simulated gastric fluid of pH 2, while hydrolyzed at a relatively higher rate in the human blood plasma to release the active parent moieties. Molecular docking analysis showed that 11 was hydrogen bonded with the Arg-31 and Gln-110 residues of the IKKß.


Assuntos
Adenocarcinoma/tratamento farmacológico , Antineoplásicos/síntese química , Antineoplásicos/farmacologia , Neoplasias Pulmonares/tratamento farmacológico , NF-kappa B/metabolismo , Ácido Oleanólico/análogos & derivados , Fator de Necrose Tumoral alfa/farmacologia , Adenocarcinoma/metabolismo , Adenocarcinoma/patologia , Antineoplásicos/química , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ensaios de Seleção de Medicamentos Antitumorais , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Simulação de Acoplamento Molecular , Estrutura Molecular , Ácido Oleanólico/síntese química , Ácido Oleanólico/química , Ácido Oleanólico/farmacologia , Relação Estrutura-Atividade
9.
Curr Top Med Chem ; 14(8): 991-1004, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24660685

RESUMO

The activation of transcription factors nuclear factor-kappa B (NF-κ B) and cyclooxygenase-2 (COX-2) is critical in cancer; they act synergistically in promoting tumor growth, survival, and resistance to chemotherapy. Thus, combined targeting of NF-κ B and COX-2 present an opportunity for synergistic anticancer efficacy. The ester prodrugs of pentacyclic triterpenoids reduced lantadene A (3), B (4), and its congener 22ß-hydroxyoleanonic acid (5) with various non steroidal anti-inflammatory drugs (NSAIDs) present a novel approach. The ester prodrugs of 3 and 4 with diclofenac showed promising dual inhibition of NF-κ B and COX-2. The lead prodrugs 14 and 15 exhibited inhibition of inhibitor of nuclear factor-kappa B kinaseß (IKKß) in the single-digit micromolar range and at the same time, prodrugs 14 and 15 showed marked cytotoxicity against A549 lung cancer cell line with IC(50s) 0.15 and 0.42 µM, respectively. The prodrugs 14 and 15 exhibited stability in the acidic pH and were hydrolyzed readily in the human blood plasma to release the active parent moieties. Thus, we have synthesized novel hybrid compounds to target both NF-κ B and COX-2 via a prodrug approach, leading to promising anticancer candidates.


Assuntos
Inibidores de Ciclo-Oxigenase 2/farmacologia , Lantana/química , NF-kappa B/antagonistas & inibidores , Ácido Oleanólico/antagonistas & inibidores , Extratos Vegetais/química , Anti-Inflamatórios não Esteroides/química , Anti-Inflamatórios não Esteroides/farmacologia , Antineoplásicos/química , Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Cristalização , Inibidores de Ciclo-Oxigenase 2/química , Humanos , Concentração de Íons de Hidrogênio , Modelos Moleculares , Estrutura Molecular , Ácido Oleanólico/análogos & derivados , Ácido Oleanólico/química , Ácido Oleanólico/farmacologia , Pró-Fármacos , Fator de Necrose Tumoral alfa
10.
Eur J Med Chem ; 74: 135-44, 2014 Mar 03.
Artigo em Inglês | MEDLINE | ID: mdl-24457265

RESUMO

The C-3, C-17 and C-22 congeners of pentacyclic triterpenoids reduced lantadene A (3), B (4) and 22ß-hydroxyoleanolic acid (5) were synthesized and were tested in vitro for their NF-κB and IKKß inhibitory potencies and cytotoxicity against A549 lung cancer cells. The lead congeners 12 and 13 showed IC50 of 0.56 and 0.42 µmol, respectively against TNF-α induced activation of NF-κB. The congeners 12 and 13 exhibited inhibition of IKKß in a single-digit micromolar dose and at the same time, 12 and 13 showed marked cytotoxicity against A549 lung cancer cells with IC50 of 0.12 and 0.08 µmol, respectively. The lead ester congeners were stable in the acidic pH, while hydrolyzed readily in the human blood plasma to release the active parent moieties.


Assuntos
Adenocarcinoma/patologia , Neoplasias Pulmonares/patologia , NF-kappa B/antagonistas & inibidores , Ácido Oleanólico/farmacologia , Adenocarcinoma/metabolismo , Linhagem Celular Tumoral , Humanos , Neoplasias Pulmonares/metabolismo , Espectroscopia de Ressonância Magnética , NF-kappa B/metabolismo , Ácido Oleanólico/química , Fosforilação , Espectrometria de Massas por Ionização por Electrospray
11.
Eur J Med Chem ; 66: 372-9, 2013 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-23827177

RESUMO

The novel 4-(4-oxo-2-arylthiazolidin-3-yl)benzenesulfonamide derivatives were designed and synthesized for selective carbonic anhydrase IX (CA IX) inhibitory activity with anticancer potential. In the CA inhibition assay, 3f was found to be the most potent and selective inhibitor of CA IX with inhibitory constant (K(I)) value of 2.2 nM. Among the synthesized compounds, 3f showed IC50 values of 5.03 µg/ml (cisplatin: 6.56 µg/ml), 5.81 µg/ml (cisplatin: 5.85 µg/ml), and 23.93 µg/ml (cisplatin: 2.75 µg/ml) against COLO-205, MDA-MB-231, and DU-145 cell lines, respectively. At IC50, 3f caused cell shrinkage, nuclear condensation, and nuclear fragmentation events characteristic to apoptosis in the Hoechst 33258 and acridine orange-ethidium bromide staining studies of COLO-205 cells. In the Dalton's lymphoma ascites (DLA) solid tumor model 3f decreased tumor volume by 64.83% (cisplatin: 71.62%), while increase in mean body weight was found to be only 4.09% (cisplatin: 3.47%).


Assuntos
Anidrases Carbônicas/metabolismo , Desenho de Fármacos , Sulfonamidas/síntese química , Sulfonamidas/farmacologia , Animais , Antígenos de Neoplasias/química , Antígenos de Neoplasias/metabolismo , Antineoplásicos/síntese química , Antineoplásicos/química , Antineoplásicos/metabolismo , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Peso Corporal/efeitos dos fármacos , Anidrase Carbônica I/química , Anidrase Carbônica I/metabolismo , Anidrase Carbônica II/química , Anidrase Carbônica II/metabolismo , Anidrase Carbônica IX , Inibidores da Anidrase Carbônica/síntese química , Inibidores da Anidrase Carbônica/química , Inibidores da Anidrase Carbônica/metabolismo , Inibidores da Anidrase Carbônica/farmacologia , Anidrases Carbônicas/química , Domínio Catalítico , Linhagem Celular Tumoral , Técnicas de Química Sintética , Humanos , Concentração Inibidora 50 , Masculino , Camundongos , Simulação de Acoplamento Molecular , Sulfonamidas/química , Sulfonamidas/metabolismo , Carga Tumoral/efeitos dos fármacos , Ensaios Antitumorais Modelo de Xenoenxerto , Benzenossulfonamidas
12.
Eur J Med Chem ; 63: 589-602, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23548704

RESUMO

Nuclear factor-kappaB (NF-κB) has been reported to regulate various genes involved in cancer and inflammation. Accordingly, drugs suppressing or inhibiting NF-κB may possess both anti-inflammatory and anticancer properties. A library of quinolone substituted thiazolidin-4-ones was docked into the active site of NF-κB and the top-ranked 31 compounds were synthesized and evaluated for anti-inflammatory and anticancer activity. The best-ranked compound 6b showed highest anti-inflammatory activity in carrageenan-induced paw edema model. In vitro anticancer studies revealed 1a and 16a as most active compounds against BT-549, HeLa, COLO-205 and ACHN human cancer cell lines. Compounds 1a and 16a exhibited NF-κB dependent anticancer properties and apoptosis mediated cell death. In vivo Ehrlich ascites carcinoma study further confirmed the antitumor activity of 1a and 16a.


Assuntos
Anti-Inflamatórios/química , Antineoplásicos/química , Quinolonas/química , Tiazolidinas/química , Animais , Anti-Inflamatórios/síntese química , Anti-Inflamatórios/farmacologia , Antineoplásicos/síntese química , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Carcinoma de Ehrlich/prevenção & controle , Carragenina , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Desenho de Fármacos , Ensaios de Seleção de Medicamentos Antitumorais , Edema/induzido quimicamente , Edema/prevenção & controle , Células HeLa , Humanos , Concentração Inibidora 50 , Camundongos , Modelos Químicos , Modelos Moleculares , Estrutura Molecular , NF-kappa B/química , NF-kappa B/metabolismo , Ligação Proteica , Estrutura Terciária de Proteína , Ratos , Tiazolidinas/síntese química , Tiazolidinas/farmacologia
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