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1.
Rev. bras. anestesiol ; 70(5): 527-533, Sept.-Oct. 2020. tab, graf
Article in English, Portuguese | LILACS | ID: biblio-1143961

ABSTRACT

Abstract Background: The current evidence suggests that oncological surgery, which is a therapy used in the treatment of solid tumors, increases the risk of metastasis. In this regard, a wide range of tumor cells express Voltage-Gated Sodium Channels (VGSC), whose biological roles are not related to the generation of action potentials. In epithelial tumor cells, VGSC are part of cellular structures named invadopodia, involved in cell proliferation, migration, and metastasis. Recent studies showed that lidocaine could decrease cancer recurrence through its direct effects on tumor cells and immunomodulatory properties on the stress response. Objective: The aim of this narrative review is to highlight the role of VGSC in tumor cells, and to describe the potential antiproliferative effect of lidocaine during the pathogenesis of metastasis. Contents: A critical review of literature from April 2017 to April 2019 was performed. Articles found on PubMed (2000-2019) were considered. A free text and MeSH-lidocaine; voltage-gated sodium channels; tumor cells; invadopodia; surgical stress; cell proliferation; metastasis; cancer recurrence - for articles in English, Spanish and Portuguese language - was used. A total of 62 were selected. Conclusion: In animal studies, lidocaine acts by blocking VGSC and other receptors, decreasing migration, invasion, and metastasis. These studies need to be replicated in humans in the context of oncological surgery.


Resumo Justificativa: As evidências atuais sugerem que a cirurgia oncológica, usada no tratamento de tumores sólidos, aumenta o risco de metástase. Nesse sentido, uma ampla gama de células tumorais expressa Canais de Sódio Dependentes de Voltagem (CSDV), cujos papéis biológicos não estão relacionados à produção de potencial de ação. Nas células epiteliais tumorais, o CSDV é parte integrante de estruturas celulares denominadas invadópodes, que participam da proliferação, migração e metástase celular. Estudos recentes mostraram que a lidocaína pode diminuir a recorrência do câncer através de efeitos diretos nas células tumorais e de propriedades imunomoduladoras na resposta ao estresse. Objetivo: O objetivo desta revisão narrativa é analisar o papel do CSDV nas células tumorais e descrever o possível efeito antiproliferativo da lidocaína na patogênese das metástases. Conteúdo: Foi realizada uma revisão crítica da literatura de Abril de 2017 a Abril de 2019. Os artigos encontrados no PubMed (2000 − 2019) foram analisados. Pesquisamos textos de linguagem livre e descritores MeSH-lidocaína; canais de sódio dependentes de voltagem; células tumorais; invadópodes; estresse cirúrgico; proliferação celular; metástase; recorrência do câncer − em artigos publicados em inglês, espanhol e português. Foram selecionadas 62 publicações. Conclusão: Em estudos empregando animais, a lidocaína atua bloqueando o CSDV e outros receptores, diminuindo a migração, invasão e metástase. Esses estudos precisam ser replicados em humanos submetidos a cirurgia oncológica.


Subject(s)
Humans , Animals , Voltage-Gated Sodium Channels/drug effects , Lidocaine/pharmacology , Neoplasms/surgery , Cell Movement/drug effects , Cell Proliferation/drug effects , Voltage-Gated Sodium Channels/metabolism , Voltage-Gated Sodium Channel Blockers/pharmacology , Neoplasm Metastasis/prevention & control , Neoplasms/pathology
2.
Braz. j. med. biol. res ; 53(1): e8659, Jan. 2020. graf
Article in English | LILACS | ID: biblio-1055485

ABSTRACT

Eosinophils are abundant in the reproductive tract, contributing to the remodeling and successful implantation of the embryo. However, the mechanisms by which eosinophils migrate into the uterus and their relationship to edema are still not entirely clear, since there are a variety of chemotactic factors that can cause migration of these cells. Therefore, to evaluate the role of CCR3 in eosinophil migration, ovariectomized C57BL/6 mice were treated with CCR3 antagonist SB 328437 and 17β-estradiol. The hypothesis that the CCR3 receptor plays an important role in eosinophil migration to the mouse uterus was confirmed, because we observed reduction in eosinophil peroxidase activity in these antagonist-treated uteruses. The antagonist also influenced uterine hypertrophy, inhibiting edema formation. Finally, histological analysis of the orcein-stained uteruses showed that the antagonist reduced eosinophil migration together with edema. These data showed that the CCR3 receptor is an important target for studies that seek to clarify the functions of these cells in uterine physiology.


Subject(s)
Animals , Female , Rabbits , Uterus/cytology , Cell Movement/drug effects , Eosinophils/drug effects , Estradiol/administration & dosage , Estrogens/administration & dosage , Receptors, CCR3/antagonists & inhibitors , Ovariectomy , Mice, Inbred C57BL
3.
Braz. j. med. biol. res ; 53(7): e9230, 2020. graf
Article in English | ColecionaSUS, LILACS, ColecionaSUS | ID: biblio-1132534

ABSTRACT

As a top leading cause of cancer death in many countries, colorectal cancer (CRC) has drawn increasing attention to the study of the pathological mechanism. According to the "cancer stem cell hypothesis", malignancies originate from a small fraction of cancer cells that show self-renewal properties to initiate and sustain tumor growth and tumor metastasis. Therefore, these cancer stem cells (CSC) probably play important roles in tumor recurrence, metastasis, and drug resistance. Previous research reported that lysine-specific histone demethylase 1 (LSD1) maintains cancer stemness through up-regulating stemness markers SOX2 and OCT4. CD133 is believed to be the most robust surface marker for CRC stem cells, however the regulatory effect of LSD1 on stemness of CD133+ CRC has never been reported. In this study, our objectives included: 1) to isolate pure CD133+ and CD133− cells from SW620 cell line; 2) to investigate the effect of LSD1 on the characteristics of CD133+ stem cancer cells by knocking down the target gene. Results suggested that the SW620 cell line had both CD133+ and CD133− subsets. The CD133+ subset exhibited more CSC-like characteristics compared with the CD133− subset with higher viability, colony formation rate, migration and invasion rate, resistance to anti-cancer drugs, and apoptosis in vitro. The CD133+ also induced faster tumor formation and larger tumors in vivo. In the LSD1-knockdown CD133+ cells, the CSC-like characteristics had been all weakened. We conclude that LSD1 was important for CSCs to maintain their "stemness" features, which could be a potential therapeutic target of CRC.


Subject(s)
Humans , Animals , Rats , Neoplastic Stem Cells/drug effects , Colorectal Neoplasms/pathology , Cell Movement/drug effects , Apoptosis/drug effects , Cell Proliferation/drug effects , Histone Demethylases/pharmacology , Neoplastic Stem Cells/metabolism , Gene Expression Regulation, Neoplastic , Blotting, Western , Colony-Forming Units Assay , Cell Line, Tumor
4.
Braz. j. med. biol. res ; 53(6): e8885, 2020. tab, graf
Article in English | ColecionaSUS, LILACS, ColecionaSUS | ID: biblio-1132519

ABSTRACT

In this study, we aimed to analyze the anti-cancer effects of β-elemene combined with paclitaxel for ovarian cancer. RT-qPCR, MTT assay, western blot, flow cytometry, and immunohistochemistry were used to analyze in vitro and in vivo anti-cancer effects of combined treatment of β-elemene and paclitaxel. The in vitro results showed that β-elemene+paclitaxel treatment markedly inhibited ovarian cancer cell growth, migration, and invasion compared to either paclitaxel or β-elemene treatment alone. Results demonstrated that β-elemene+paclitaxel induced apoptosis of SKOV3 cells, down-regulated anti-apoptotic Bcl-2 and Bcl-xl gene expression and up-regulated pro-apoptotic P53 and Apaf1 gene expression in SKOV3 cells. Administration of β-elemene+paclitaxel arrested SKOV3 cell cycle at S phase and down-regulated CDK1, cyclin-B1, and P27 gene expression and apoptotic-related resistant gene expression of MDR1, LRP, and TS in SKOV3 cells. In vivo experiments showed that treatment with β-elemene+paclitaxel significantly inhibited ovarian tumor growth and prolonged the overall survival of SKOV3-bearing mice. In addition, the treatment inhibited phosphorylated STAT3 and NF-κB expression in vitro and in vivo. Furthermore, it inhibited migration and invasion through down-regulation of the STAT-NF-κB signaling pathway in SKOV3 cells. In conclusion, the data suggested that β-elemene+paclitaxel can inhibit ovarian cancer growth via down-regulation of the STAT3-NF-κB signaling pathway, which may be a potential therapeutic strategy for ovarian cancer therapy.


Subject(s)
Animals , Male , Female , Rabbits , Ovarian Neoplasms/drug therapy , Sesquiterpenes/administration & dosage , Cell Movement/drug effects , NF-kappa B/adverse effects , Paclitaxel/administration & dosage , Apoptosis/drug effects , Cell Proliferation/drug effects , Ovarian Neoplasms/metabolism , Ovarian Neoplasms/pathology , Immunohistochemistry , Transfection , Signal Transduction , Blotting, Western , NF-kappa B/metabolism , Cell Line, Tumor , Real-Time Polymerase Chain Reaction , Mice, Inbred BALB C
5.
Article in Chinese | WPRIM | ID: wpr-879924

ABSTRACT

Endothelial progenitor cells (EPCs) play an important role in diabetic vascular complications. A large number of studies have revealed that some clinical antihyperglycemics can improve the complications of diabetes by regulating the function of EPCs. Metformin can improve EPCs function in diabetic patients by regulating oxidative stress level or downstream signaling pathway of adenosine monophosphate activated protein kinase; Pioglitazone can delay the aging of EPCs by regulating telomerase activity; acarbose, sitagliptin and insulin can promote the proliferation, migration and adhesion of EPCs. In addition to lowering blood glucose, the effects of antihyperglycemics on EPCs may also be one of the mechanisms to improve the complications of diabetes. This article reviews the research progress on the regulation of EPC proliferation and function by antihyperglycemics.


Subject(s)
Cell Movement/drug effects , Cells, Cultured , Endothelial Progenitor Cells/drug effects , Humans , Hypoglycemic Agents/pharmacology , Signal Transduction/drug effects
6.
Braz. j. otorhinolaryngol. (Impr.) ; 85(6): 705-715, Nov.-Dec. 2019. tab, graf
Article in English | LILACS | ID: biblio-1055510

ABSTRACT

Abstract Introduction: Serum- and glucocorticoid-inducible kinase 3, a serine/threonine kinase that functions downstream of the PI3K signaling pathway, plays a critical role in neoplastic processes. It is expressed by various tumors and contributes to carcinogenesis. Objective: The objective was to investigate serum- and glucocorticoid-inducible kinase 3 expression in nasopharyngeal carcinoma, to study the anti-tumor effects of serum- and glucocorticoid-inducible kinase 3 shRNA by inhibiting its expression in nasopharyngeal carcinoma cells and to discuss the potential implications of our findings. Methods: Serum- and glucocorticoid-inducible kinase 3 protein expression in nasopharyngeal carcinoma cell lines (CNE-1, CNE-2, HNE-1, HONE-1, and SUNE-1) and the human immortalized nasopharyngeal epithelium cell line NP69 were assayed by western blotting. Serum- and glucocorticoid-inducible kinase 3 expression in 42 paraffin-embedded nasopharyngeal carcinoma tissues were performed by immunohistochemistry. MTT assay, flow cytometry, and scratch tests were performed after CNE-2 cells were transfected with the best serum- and glucocorticoid-inducible kinase 3 shRNA plasmid selected by western blotting using lipofectamine to study its effect on cell proliferation, apoptosis, and migration. Results: Serum- and glucocorticoid-inducible kinase 3 was overexpressed in human nasopharyngeal carcinoma tissues and cells. Serum- and glucocorticoid-inducible kinase 3 expression decreased markedly after CNE-2 cells were transfected with the serum- and glucocorticoid-inducible kinase 3 shRNA, leading to strong inhibition of cell proliferation and migration. In addition, the apoptosis rate increased in CNE-2 cells after serum- and glucocorticoid-inducible kinase 3 knockdown. Conclusion: Serum- and glucocorticoid-inducible kinase 3 expression was more frequently observed as the nasopharyngeal epithelium progresses from normal tissue to carcinoma. This suggests that serum- and glucocorticoid-inducible kinase 3 contributes to the multistep process of NPC carcinogenesis. Serum- and glucocorticoid-inducible kinase 3 represents a target for nasopharyngeal carcinoma therapy, and a basis exists for the further investigation of this adjuvant treatment modality for nasopharyngeal carcinoma.


Resumo Introdução: A quinase 3 sérica induzida por glicocorticoide, uma serina/treonina quinase que funciona downstream da via de sinalização PI3K, desempenha um papel crítico nos processos neoplásicos. É expressa por vários tumores e contribui para a carcinogênese. Objetivo: Investigar a expressão de quinase 3 sérica induzida por glicocorticoide no carcinoma nasofaríngeo, estudar os efeitos antitumorais do shRNA da quinase 3 sérica induzida por glicocorticoide, que inibem sua expressão em células de carcinoma nasofaríngeo, e discutir as implicações potenciais de nossos achados. Método: A expressão de proteína quinase 3 sérica induzida por glicocorticoide em linhagens de células de carcinoma nasofaríngeo (CNE-1, CNE-2, HNE-1, HONE-1 e SUNE-1) e a linhagem de células humanas imortalizadas do epitélio nasofaríngeo NP69 foram avaliadas por Western blot. A expressão da quinase 3 sérica induzida por glicocorticoide em 42 tecidos de CNF embebidos em parafina foi feita por imuno-histoquímica. Testes com MTT, citometria de fluxo e testes de raspagem foram feitos após as células CNE-2 terem sido transfectadas com o melhor plasmídeo shRNA da quinase 3 sérica induzida por glicocorticoide selecionado por Western blot, com o uso de lipofectamina para estudar seu efeito na proliferação, apoptose e migração celular. Resultados: Foi observada uma sobre-expressão da quinase 3 sérica induzida por glicocorticoide em tecidos e células de carcinoma nasofaríngeo humanas. A expressão de quinase 3 sérica induzida por glicocorticoide diminuiu acentuadamente após as células CNE-2 terem sido transfectadas com o shRNA da quinase 3 sérica induzida por glicocorticoide, conduzindo a forte inibição de proliferação e migração celular. Além disso, a taxa de apoptose aumentou nas células CNE-2 após o knockdown da quinase 3 sérica induzida por glicocorticoide. Conclusão: A expressão de quinase 3 sérica induzida por glicocorticoide foi observada com maior frequência à medida que o epitélio nasofaríngeo progride de tecido normal para carcinoma. Isso sugere que a quinase 3 sérica induzida por glicocorticoide contribui para o processo multietapas da carcinogênese do carcinoma nasofaríngeo. A quinase 3 sérica induzida por glicocorticoide representa um alvo para a terapia do carcinoma nasofaríngeo e há uma base para a investigação adicional dessa modalidade de tratamento adjuvante para o carcinoma nasofaríngeo.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Nasopharyngeal Neoplasms/metabolism , Protein-Serine-Threonine Kinases/metabolism , Immediate-Early Proteins/metabolism , Nasopharyngeal Carcinoma/metabolism , Immunohistochemistry , Cell Movement/drug effects , Nasopharyngeal Neoplasms/pathology , Nasopharyngitis/metabolism , Nasopharyngitis/pathology , Protein-Serine-Threonine Kinases/pharmacology , Apoptosis , Immediate-Early Proteins/pharmacology , RNA, Small Interfering/metabolism , Cell Proliferation/drug effects , Nasopharyngeal Carcinoma/pathology
7.
Arq. bras. oftalmol ; 82(1): 38-44, Jan.-Feb. 2019. tab, graf
Article in English | LILACS | ID: biblio-973869

ABSTRACT

ABSTRACT Purpose: To evaluate the effects of ranibizumab and amfenac in human uveal melanoma cell lines and to explore the ability of these compounds to sensitize uveal melanoma cells to radiation therapy. Methods: The 92.1 human uveal melanoma cell line was cultured and subjected to the proposed treatment (ranibizumab, amfenac, and a combination of both). Proliferation, migration, and invasion assays of the 92.1 uveal melanoma cell line were assessed after pretreatment with ranibizumab (125 mg/mL), amfenac (150 nM), or a combination of both. In addition, proliferation rates were assessed after treatment with ranibizumab and amfenac, and the cells were subsequently exposed to various radiation doses (0, 4, and 8 Gy). Results: Proliferation assay: cells treated with a combination of ranibizumab and amfenac had lower proliferation rates than controls (p=0.016) and than those treated with only ranibizumab (p=0.033). Migration assay: a significantly lower migration rate was observed in cells treated with amfenac than the control (p=0.014) and than those treated with ranibizumab (p=0.044). Invasion assay: there were no significant differences among the studied groups. Irradiation exposure: in the 4 Gy dose group, there were no significant differences among any groups. In the 8 Gy dose group, treatment with ranibizumab, amfenac, and their combination prior to application of the 8 Gy radiation led to a marked reduction in proliferation rates (p=0.009, p=0.01, and p=0.034, respectively) compared with controls. Conclusion: Combination of ranibizumab and amfenac reduced the proliferation rate of uveal melanoma cells; however, only amfenac monotherapy significantly decreased cell migration. The radiosensitivity of the 92.1 uveal melanoma cell line increased following the administration of ranibizumab, amfenac, and their combination. Further investigation is warranted to determine if this is a viable pretreatment strategy to render large tumors amenable to radiotherapy.


RESUMO Objetivo: Avaliar os efeitos do ranibizumabe em associação com o amfenac nas células de melanoma uveal humano e explorar a capacidade desses compostos em sensibilizar as células de melanoma uveal à radioterapia. Métodos: Células de melanoma uveal humano do tipo 92.1 foram cultivadas e submetidas ao tratamento proposto (ranibizumabe, amfenac e a combinação de ambos). Ensaios de proliferação, migração e invasão com as células de melanoma uveal do tipo 92.1 foram avaliados após tratamento com ranibizumabe (125 mg/ml), amfenac (150 nM) e a combinação de ambos. Além disso, as taxas de proliferação foram avaliadas após tratamento com ranibizumabe e amfenac com subsequente exposição das células a diferentes doses de radiação (0 Gy, 4 Gy e 8 Gy). Resultados: Ensaio de proliferação: células tratadas com ranibizumabe e amfenac combinados apresentaram taxas de proliferação inferiores em comparação ao grupo controle (p=0,016), do que as tratadas apenas com ranibizumabe (p=0,033). Ensaio de migração: foi observada uma taxa de migração significativamente mais baixa nas células tratadas com amfenac do que no grupo controle (p=0,014) e do que nas tratadas com ranibizumabe (p=0,044). Ensaio de invasão: não houve diferenças significativas entre os grupos estudados. Exposição à irradiação: no grupo da dose de 4 Gy, não houve diferença significante entre os grupos. No grupo da dose de 8 Gy, o tratamento com ranibizumabe, afenac e sua combinação antes da aplicação da radiação de 8 Gy levou a uma redução acentuada nas taxas de proliferação (p=0,009, p=0,01 e p=0,034, respectivamente) em comparação aos grupos controle. Conclusão: A combinação de ranibizumabe e amfenac reduziu a taxa de proliferação das células de melanoma uveal; no entanto, apenas o amfenac diminuiu significativamente a migração celular. A radiossensibilidade das células de melanoma uveal do tipo 92.1 aumentou após a administração de ranibizumabe, amfenac e sua combinação. Mais investigações são necessárias para determinar se esta é uma estratégia de pré-tratamento viável para tornar grandes tumores passíveis de radioterapia.


Subject(s)
Humans , Phenylacetates/pharmacology , Angiogenesis Inhibitors/pharmacology , Cyclooxygenase 2 Inhibitors/pharmacology , Ranibizumab/pharmacology , Melanoma/drug therapy , Melanoma/radiotherapy , Radiation Tolerance , Uveal Neoplasms/drug therapy , Uveal Neoplasms/radiotherapy , Antineoplastic Combined Chemotherapy Protocols , Cell Movement/drug effects , Cell Movement/radiation effects , Reproducibility of Results , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Proliferation/radiation effects , Dose-Response Relationship, Radiation
8.
Braz. j. med. biol. res ; 52(4): e8409, 2019. graf
Article in English | LILACS | ID: biblio-1001514

ABSTRACT

Benzyl isothiocyanate (BITC) has been shown to inhibit invasion and induce apoptosis of various types of cancer. However, its role on human oral squamous cell carcinoma (OSCC) cells is still not well elucidated. In the present study, we investigated the effect of BITC on apoptosis and invasion of SCC9 cells, and its underlying mechanisms in vitro and in vivo. SCC9 cells were exposed to BITC (5 and 25 μM) for 24 and 48 h. Cell growth, apoptosis, invasion, and migration were detected in vitro by MTT, FITC-conjugated annexin V/propidium iodide staining followed by flow cytometry, Matrigel-coated semi-permeable modified Boyden, and wound-healing assay. S100A4, PUMA, and MMP-9 expressions were detected to investigate its mechanisms. Xenotransplantation experiments were used to investigate the role of BITC on tumor growth and lung metastasis. BITC inhibited cell viability and induced cell apoptosis in a dose- and time-dependent manner through upregulation of PUMA signals. BITC inhibited cell invasion and migration by downregulation of S100A4 dependent MMP-9 signals. The ip administration of BITC reduced tumor growth but not lung metastasis of SCC9 cells subcutaneously implanted in nude mice. BITC treatment activated pro-apoptotic PUMA and inhibited S100A4-dependent MMP-9 signals, resulting in the inhibition of cell growth and invasion in cultured and xenografted SCC9 cells. Thereby, BITC is a potential therapeutic approach for OSCC.


Subject(s)
Animals , Female , Rabbits , Carcinoma, Squamous Cell/pathology , Cell Movement/drug effects , Apoptosis/drug effects , Isothiocyanates/pharmacology , Cell Proliferation/drug effects , S100 Calcium-Binding Protein A4/drug effects , Immunohistochemistry , Cell Survival/drug effects , Cell Line, Tumor , S100 Calcium-Binding Protein A4/metabolism , Mice, Nude
9.
Braz. j. med. biol. res ; 52(2): e8209, 2019. tab, graf
Article in English | LILACS | ID: biblio-984033

ABSTRACT

Vegetable oils have been used for a plethora of health benefits by their incorporation in foods, cosmetics, and pharmaceutical products, especially those intended for skin care. This study aimed to investigate the cutaneous benefits of a vegetable oil blend (VOB) formulation and its fatty acid composition. The anti-inflammatory activity was studied in macrophages of RAW 264.7 cells by investigating the release of nitric oxide (NO), superoxide anion generation (O2-), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6). ABTS cation radical scavenging capacity assay, ferric reducing antioxidant potential (FRAP), 2,2-diphenyl-1-picrylhydrazyl (DPPH), and NO free radical scavenging assays were used to evaluate the antioxidant activity. VOB was tested for its ability to stimulate fibroblast proliferation and migration using the scratch assay, and antibacterial activity by the microdilution test. The fatty acid profile of a freshly prepared VOB formulation was determined by gas chromatography before and after accelerated stability testing. Chemical composition of VOB revealed the presence of oleic acid (C18:1n-9; 63.3%), linoleic acid (C18:2n-6; 4.7%), and linolenic acid (C18:3n-6; 5.1%) as major mono- and polyunsaturated fatty acids. No changes in the organoleptic characteristics and fatty acid composition were observed after the accelerated stability test. VOB 100 µg/mL reduced the healing time by increasing the total number of cells in the wounded area by 43.0±5.1% compared to the negative control group. VOB also suppressed the pro-inflammatory TNF-α and IL-6 cytokines, and NO and O2- production in lipopolysaccharide-stimulated macrophage cells. In conclusion, the VOB formulation contributed to the improvement of current therapeutic strategies for cutaneous applications in skin care.


Subject(s)
Animals , Rabbits , Wound Healing/drug effects , Plant Oils/pharmacology , Fatty Acids/pharmacology , Anti-Inflammatory Agents/pharmacology , Anti-Bacterial Agents/pharmacology , Antioxidants/pharmacology , Plant Oils/chemistry , Cell Movement/drug effects , Cells, Cultured , Skin Care , Cell Proliferation/drug effects , Fibroblasts/drug effects
10.
Braz. j. med. biol. res ; 52(12): e8934, 2019. graf
Article in English | LILACS | ID: biblio-1055468

ABSTRACT

Baicalein (BAI) is an acknowledged flavonoids compound, which is regarded as a useful therapeutic pharmaceutical for numerous cancers. However, its involvement in melanoma is largely unknown. This study aimed to examine the anti-melanoma function of BAI and unraveled the regulatory mechanism involved. A375 and SK-MEL-28 were treated with BAI for 24 h. Then, CCK-8 assay, flow cytometry, and transwell assay were carried out to investigate cell growth, migration, and invasion. RT-qPCR was applied to detect the expression of colon cancer associated transcript-1 (CCAT1) in melanoma tissues and cells. The functions of CCAT1 in melanoma cells were also evaluated. Western blot was utilized to appraise Wnt/β-catenin or MEK/ERK pathways. BAI restrained cell proliferation and stimulated cell apoptotic capability of melanoma by suppressing cleaved-caspase-3 and cleaved-PARP. Cell migratory and invasive abilities were restrained by BAI via inhibiting MMP-2 and vimentin. CCAT1 was over-expressed in melanoma tissues and down-regulated by BAI in melanoma cells. Overexpressed CCAT1 reversed the BAI-induced anti-growth, anti-migratory, and anti-invasive effects. Furthermore, BAI inhibited Wnt/β-catenin and MEK/ERK pathways-axis via regulating CCAT1. Our study indicated that BAI blocked Wnt/β-catenin and MEK/ERK pathways via regulating CCAT1, thereby inhibiting melanoma cell proliferation, migration, and invasion.


Subject(s)
Humans , Gene Expression Regulation, Neoplastic/drug effects , Flavanones/pharmacology , RNA, Long Noncoding/metabolism , Melanoma/pathology , Down-Regulation/drug effects , Cell Movement/drug effects , Blotting, Western , Reverse Transcriptase Polymerase Chain Reaction , Cell Line, Tumor , Cell Proliferation/drug effects , Real-Time Polymerase Chain Reaction , Neoplasm Invasiveness
11.
Braz. j. med. biol. res ; 52(10): e8385, 2019. graf
Article in English | LILACS | ID: biblio-1039242

ABSTRACT

Malignant melanoma (MM) is one of the malignant tumors with highly metastatic and aggressive biological actions. Schizandrin A (SchA) is a bioactive lignin compound with strong anti-oxidant and anti-aging properties, which is stable at room temperature and is often stored in a cool dry place. Hence, we investigated the effects of SchA on MM cell line A375 and its underlying mechanism. A375 cells were used to construct an in vitro MM cell model. Cell viability, proliferation, apoptosis, and migration were detected by Cell Counting Kit-8, BrdU assay, flow cytometry, and transwell two-chamber assay, respectively. The cell cycle-related protein cyclin D1 and cell apoptotic proteins (Bcl-2, Bax, cleaved-caspase-3, and cleaved-caspase-9) were analyzed by western blot. Alteration of H19 expression was achieved by transfecting with pEX-H19. PI3K/AKT pathway was measured by detecting phosphorylation of PI3K and AKT. SchA significantly decreased cell viability in a dose-dependent manner. Furthermore, SchA inhibited cell proliferation and cyclin D1 expression. SchA increased cell apoptosis along with the up-regulation of pro-apoptotic proteins (cleaved-caspase-3, cleaved-caspase-9, and Bax) and the down-regulation of anti-apoptotic protein (Bcl-2). Besides, SchA decreased migration and down-regulated matrix metalloproteinases (MMP)-2 and MMP-9. SchA down-regulated lncRNA H19. Overexpression of H19 blockaded the inhibitory effects of SchA on A375 cells. SchA decreased the phosphorylation of PI3K and AKT while H19 overexpression promoted the phosphorylation of PI3K and AKT. SchA inhibited A375 cell growth, migration, and the PI3K/AKT pathway through down-regulating H19.


Subject(s)
Humans , Polycyclic Compounds/pharmacology , Down-Regulation/drug effects , Cell Movement/drug effects , Apoptosis/drug effects , Lignans/pharmacology , Cyclooctanes/pharmacology , Cell Proliferation/drug effects , Melanoma/pathology , Signal Transduction/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Blotting, Western , MicroRNAs/metabolism , Cell Line, Tumor , Real-Time Polymerase Chain Reaction , RNA, Long Noncoding
12.
Braz. oral res. (Online) ; 33: e117, 2019. tab, graf
Article in English | LILACS, BBO | ID: biblio-1132651

ABSTRACT

Abstract: The aim of this study was to evaluate the effect of mineral trioxide aggregate (MTA) and Brazilian propolis on the cell viability, mineralization, anti-inflammatory ability, and migration of human dental pulp cells (hDPCs). The cell viability was evaluated with CCK-8 kit after 1, 5, 7, and 9 days. The deposition of calcified matrix and the expression of osteogenesis-related genes were evaluated by Alizarin Red staining and real-time PCR after incubation in osteogenic medium for 21 days. The expression of inflammation-related genes in cells was determined after exposure to 1 μg/mL LPS for 3 h. Finally, the numbers of cells that migrated through the permeable membranes were compared during 15 h. Propolis and MTA significantly increased the viability of hDPCscompared to the control group on days 7 and 9. In the propolis group, significant enhancement of osteogenic potential and suppressed expression of IL-1β and IL-6 was observed after LPS exposure compared to the MTA and control groups. The number of migration cells in the propolis group was similar to that of the control group, while MTA significantly promoted cell migration. Propolis showed comparable cell viability to that of MTA and exhibited significantly higher anti-inflammatory and mineralization promotion effects on hDPCs.


Subject(s)
Humans , Oxides/pharmacology , Propolis/pharmacology , Silicates/pharmacology , Calcium Compounds/pharmacology , Aluminum Compounds/pharmacology , Dental Pulp/cytology , Dental Pulp/drug effects , Anti-Inflammatory Agents/pharmacology , Brazil , Cell Movement/drug effects , Cell Survival/drug effects , Cells, Cultured , Reproducibility of Results , Anthraquinones , Interleukin-6/analysis , Tumor Necrosis Factor-alpha , Statistics, Nonparametric , Drug Combinations , Interleukin-1beta/analysis , Real-Time Polymerase Chain Reaction , Odontoblasts/drug effects
13.
Bol. latinoam. Caribe plantas med. aromát ; 17(6): 575-582, nov. 2018. ilus
Article in English | LILACS | ID: biblio-1007341

ABSTRACT

The skin is the largest organ of the human body and its main function is to protect it from the external environment. It is exposed to injuries that require a rapid healing process to recover its functionality. Microorganisms inhabit the skin, which makes up the normal microbial flora, but in situations of injury they can cause infections that slow down the regeneration process. Therefore, there is a great interest in the development of alternative methods to accelerate the regeneration process and prevent infections. In this work, the efficacy of flavonoid 3-O-methylgalangine and the terpenic derivative Filifolinone and its mixtures, isolated from plants of the genus Heliotropium, on the stimulation of cell proliferation was evaluated. The results showed that the mixtures stimulated proliferation and migration in MA104 cells mainly due to the presence of Filifolinone, that together with the known antibacterial activity of 3-O-methylgalangine, opens new alternatives for the use of natural compounds in healing processes.


La piel es el órgano más grande del cuerpo humano y su función principal es protegerla del entorno externo. Está expuesta a lesiones que requieren un proceso de curación rápido para recuperar su funcionalidad. Los microorganismos que habitan en la piel, constituyen la flora microbiana normal, pero en situaciones de lesión pueden causar infecciones que retardan el proceso de regeneración. Por lo tanto, existe un gran interés en el desarrollo de métodos alternativos para acelerar el proceso de regeneración y prevenir infecciones. En este trabajo, se evaluó la eficacia del flavonoide 3-O-metilgalangina y el derivado terpénico Filifolinona y sus mezclas, aisladas de plantas del género Heliotropium, en la estimulación de la proliferación celular. Los resultados mostraron que las mezclas estimularon la proliferación y la migración en las células MA104 debido principalmente a la presencia de Filifolinona, que junto con la actividad antibacteriana conocida de la 3-O-metilgalangina, abre nuevas alternativas para el uso de compuestos naturales en los procesos de curación.


Subject(s)
Terpenes/pharmacology , Flavonoids/pharmacology , Heliotropium , Cell Proliferation/drug effects , Terpenes/chemistry , Wound Healing , Flavonoids/chemistry , Cell Movement/drug effects , Cell Survival/drug effects , Cells, Cultured , Epithelial Cells/drug effects
14.
Braz. j. med. biol. res ; 51(4): e6803, 2018. graf
Article in English | LILACS | ID: biblio-889059

ABSTRACT

Propofol is an intravenous sedative hypnotic agent of which the growth-inhibitory effect has been reported on various cancers. However, the roles of propofol in endometrial cancer (EC) remain unclear. This study aimed to explore the effects of propofol on EC in vitro and in vivo. Different concentrations of propofol were used to treat Ishikawa cells. Colony number, cell viability, cell cycle, apoptosis, migration, and invasion were analyzed by colony formation, MTT, flow cytometry, and Transwell assays. In addition, the pcDNA3.1-Sox4 and Sox4 siRNA plasmids were transfected into Ishikawa cells to explore the relationship between propofol and Sox4 in EC cell proliferation. Tumor weight in vivo was measured by xenograft tumor model assay. Protein levels of cell cycle-related factors, apoptosis-related factors, matrix metalloproteinases 9 (MMP9), matrix metalloproteinases 2 (MMP2) and Wnt/β-catenin pathway were examined by western blot. Results showed that propofol significantly decreased colony numbers, inhibited cell viability, migration, and invasion but promoted apoptosis in a dose-dependent manner in Ishikawa cells. Moreover, propofol reduced the expression of Sox4 in a dose-dependent manner. Additionally, propofol significantly suppressed the proportions of Ki67+ cells, but Sox4 overexpression reversed the results. Furthermore, in vivo assay results showed that propofol inhibited tumor growth; however, the inhibitory effect was abolished by Sox4 overexpression. Moreover, propofol inhibited Sox4 expression via inactivation of Wnt/β-catenin signal pathway. Our study demonstrated that propofol inhibited cell proliferation, migration, and invasion but promoted apoptosis by regulation of Sox4 in EC cells. These findings might indicate a novel treatment strategy for EC.


Subject(s)
Animals , Female , Apoptosis/drug effects , Endometrial Neoplasms/drug therapy , Hypnotics and Sedatives/pharmacology , Propofol/pharmacology , SOXC Transcription Factors/metabolism , beta Catenin/metabolism , Cell Line, Tumor , Cell Movement/drug effects , Cell Survival/drug effects , Endometrial Neoplasms/pathology , Mice, Inbred BALB C , Neoplasm Invasiveness , Propofol/administration & dosage , Tumor Stem Cell Assay , Wnt Proteins/metabolism , Xenograft Model Antitumor Assays
15.
Braz. j. med. biol. res ; 51(4): e6867, 2018. graf
Article in English | LILACS | ID: biblio-889068

ABSTRACT

Polydatin, a small molecule from Polygonum cuspidatum, has many biological functions, particularly anti-cancer effects. However, the anti-cancer effects of polydatin in hepatocellular carcinoma (HCC) have not been examined yet. In the present study, MTT assay, BrdU assay, transwell invasion assay, and wound healing assay were performed to determine cell proliferation, invasion and migration. Flow cytometry and TUNEL assay were used to measure cell apoptosis. Quantitative real-time PCR and western blotting assays were used to determine mRNA and protein expression levels. Xenograft experiment was performed to determine the in vivo anti-tumor effect of polydatin. Immunostaining was performed to analyze the expression of caspase-3 and Ki-67. Our results showed that polydatin inhibited cell proliferation in a concentration-dependent and time-dependent manner in the HCC cell lines. Polydatin also induced cell apoptosis in a concentration-dependent manner possibly via increasing the caspase-3 activity, and up-regulating the protein expression of caspase-3, caspase-9, Bax, and down-regulating the protein expression of Bcl-2. In addition, polydatin treatment had an inhibitory effect on cell proliferation, invasion and migration in HCC cell lines. Polydatin treatment also suppressed the Wnt/beta-catenin signaling activities in HCC cells. Polydatin treatment significantly reduced tumor growth in nude mice inoculated with HepG2 cells, suppressed the expression of Ki-67, and increased caspase-3 expression and TUNEL activity. Our data indicated the important role of polydatin for the suppression of HCC progression.


Subject(s)
Animals , Male , Mice , Stilbenes/pharmacology , Cell Movement/drug effects , Apoptosis/drug effects , Carcinoma, Hepatocellular/drug therapy , Cell Proliferation/drug effects , Glucosides/pharmacology , Liver Neoplasms, Experimental/drug therapy , Drugs, Chinese Herbal , Blotting, Western , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Real-Time Polymerase Chain Reaction , Flow Cytometry , Liver Neoplasms, Experimental/pathology , Mice, Inbred BALB C , Mice, Nude , Neoplasm Invasiveness
16.
Bauru; s.n; 2018. 98 p. ilus, graf, tab.
Thesis in Portuguese | LILACS, BBO | ID: biblio-885097

ABSTRACT

O osteossarcoma (OS) é o tumor maligno primário mais comum do tecido ósseo, caracterizado pela formação de osteócitos anormais. Apesar do avanço nas terapias convencionais (quimioterapia e retirada do tumor), essas não conseguem eliminar totalmente as células tumorais e impedir a progressão da doença. Recentemente, agentes derivados de fontes naturais ganharam considerável atenção por causa de sua segurança, eficácia e disponibilidade imediata. Nesse sentido, a apocinina, inibidor do complexo NADPH-oxidase, vem sendo estudada como agente antitumoral em alguns tipos de câncer como: pâncreas, próstata, pulmão e mama. Apocinina é um pró-fármaco e sua ação parece estar relacionada à sua conversão produzindo a diapocinina, a qual se mostrou mais efetiva do que a apocinina. Portanto, o objetivo desse estudo é avaliar, in vitro, o potencial antitumoral da apocinina e diapocinina em células de osteossarcoma humano. Para isso, foram utilizados osteoblastos humanos normais (HOb) e osteossarcoma humano imortalizadas (SaOS-2) tratados ou não com apocinina e diapocinina em diversas concentrações. Foram realizados os ensaios de viabilidade celular, alterações morfológicas, apoptose celular, produção de espécies reativas de oxigênio (EROs), formação de colônias, migração, invasão e expressão do fator indutor de hipóxia-1alfa (HIF-1). Também foram conduzidos ensaios para verificar a atividade de metaloproteinase de matriz (MMP) 2 e 9. Os resultados em SaOS-2 mostraram que o tratamento com apocinina nas concentrações de 1,5 e 3 mM; e diapocinina nas concentrações de 0,75 e 1,5 mM reduziram a viabilidade; aumentaram o número de células em apoptose e diminuíram a produção de EROs; sem causar danos às células HOb. Além disso, essas mesmas concentrações inibiram a migração e invasão celular; diminuíram a expressão de HIF-1; e reduziram a atividade de MMP-2 em SaOS-2. Considerando os resultados obtidos, concluímos que a apocinina e diapocinina podem atuar como possíveis moduladores de células tumorais, sendo que a diapocinina mostrou ser mais efetiva nos parâmetros testados.(AU)


Osteosarcoma (OS) is the most common primary malignant tumor of bone tissue, characterized by the formation of abnormal osteocytes. Despite advances in conventional therapies (chemotherapy and surgery) they cannot completely eliminate tumor cells and prevent the progression of the disease. Recently, agents derived from natural sources have achieved considerable attention because of their safety, efficacy and immediate availability of therapies. In this way, apocynin, an inhibitor of the NADPH-oxidase complex, has been studied as an antitumor agent in some types of cancer, such as pancreas, prostate, lung and breast. Apocynin is a prodrug and its action indicate to be related to its conversion to diapocynin, which has been shown to be more efficient than apocynin itself. Thus, the aim of this study is to evaluate, in vitro, the antitumor potential of apocynin and diapocynin in human osteosarcoma cells. For this, normal human osteoblasts (HOb) and immortalized human osteosarcoma cells (SaOS-2) were treated or no-treated with apocynin and diapocynin in various concentrations. Cell viability assay, morphological alterations, cellular apoptosis, reactive oxygen species (ROS) production, colony formation, migration, invasion and expression of hypoxia-inducible factor-1 alpha (HIF-1) were performed. We also performed assays to verify the activity of matrix metalloproteinase (MMP) 2 and 9. The results in SaOS-2 showed that treatment with apocynin at concentrations of 1,5 e 3 mM; and diapocynin at concentrations of 0,75 e 1,5 mM reduced cell viability; increased the number of cells in apoptosis and decreased the production of ROS; without damaging HOb cells. Moreover, these same concentrations inhibited cell migration and invasion; decreased HIF-1 expression; and reduced MMP 2 activity in SaOS-2. Considering the results, we suggest that apocynin and diapocynin may act as possible modulators of tumor cells, and diapocynin has been shown to be more effective.(AU)


Subject(s)
Humans , Acetophenones/pharmacology , Antineoplastic Agents/pharmacology , Biphenyl Compounds/pharmacology , Osteosarcoma/drug therapy , Apoptosis/drug effects , Cell Movement/drug effects , Cell Survival/drug effects , Matrix Metalloproteinase 2/drug effects , Matrix Metalloproteinase 9/drug effects , Osteoblasts/drug effects , Reactive Oxygen Species/analysis , Reproducibility of Results , Tumor Cells, Cultured
17.
Biol. Res ; 51: 14, 2018. graf
Article in English | LILACS | ID: biblio-950900

ABSTRACT

BACKGROUND: Neurokinin1 (NK1) receptor has played a vital role in the development of tumor. However, NKP608 as a NK1 receptor antagonist whether has the effect of the resistance of colorectal cancer is still unclear. Thereby, in this study, we investigated the role of NKP608 on human colorectal cancer and explored the underlying mechanism. METHODS: The cell proliferation of colorectal cancer cells was detected by cell counting kit-8 (CCK8) assay, cell migration and invasion were assessed by transwell assay, the apoptotic ratio of cells was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide stained and flow cytometry. The involvement of molecular mechanisms was examined by western blot. RESULTS: In this study, we found that NKP608 inhibited the proliferation, migration/invasion of HCT116 cells. In addition, NKP608 reduced expressions of Wnt-3a, ß-catenin, Cyclin D1, and (vascular endothelial growth factor) VEGF while induced expression of E-Cadherin. Furthermore, flow cytometry analyzed that NKP608 induced apoptosis of HCT116 cells, consistently, western blotting detecting of apoptosis-related proteins revealed that NKP608 downregulated Bcl-2 while upregulated Bax and Active-Caspase-3. CONCLUSIONS: Taken together, our results demonstrated that NKP608 inhibited colorectal cancer cell proliferation, migration and invasion via suppressing the Wnt/ß-catenin signaling pathway. Therefore, NKP608 might represent a promising therapeutic agent in the treatment of colorectal cancer.


Subject(s)
Humans , Piperidines/pharmacology , Quinolines/pharmacology , Colorectal Neoplasms/pathology , Cell Movement/drug effects , Cell Proliferation/drug effects , Wnt Signaling Pathway/drug effects , Neurokinin-1 Receptor Antagonists/pharmacology , Down-Regulation/drug effects , Blotting, Western , Cell Line, Tumor , HCT116 Cells , Flow Cytometry
18.
Braz. j. med. biol. res ; 51(1): e6799, 2018. tab, graf
Article in English | LILACS | ID: biblio-889013

ABSTRACT

Arthritis is positively associated with the decline of sex hormones, especially estrogen. Tamoxifen (TMX) is a selective estrogen receptor modulator, possessing agonist or antagonistic activity in different tissues. Thus, the objective of this study was to investigate the effect of TMX on the zymosan-induced arthritis model. Female Swiss normal and ovariectomized (OVX) mice were divided into groups and treated for five days with TMX (0.3, 0.9 or 2.7 mg/kg) or 17-β-estradiol (E2, 50 µg/kg). On the fifth day, arthritis was induced and 4 h later, leukocyte migration into joint cavities was evaluated. The neutrophil migration in OVX animals, but not in normal mice, treated with TMX (all tested doses) was significantly decreased compared with mice that received the vehicle (P≤0.05). Similarly, this effect was also demonstrated in the E2-treated group. Therefore, the present study demonstrates that TMX presented agonist effects in inhibiting neutrophil migration and preventing arthritis progression in OVX mice.


Subject(s)
Animals , Female , Rabbits , Arthritis, Experimental/drug therapy , Tamoxifen/pharmacology , Ovariectomy , Selective Estrogen Receptor Modulators/pharmacology , Organ Size/drug effects , Time Factors , Uterus/drug effects , Zymosan , Cell Movement/drug effects , Treatment Outcome , Estrous Cycle/drug effects , Disease Models, Animal , Estrogen Antagonists/pharmacology , Cell Migration Assays, Leukocyte , Neutrophils/drug effects
19.
J. appl. oral sci ; 26: e20180077, 2018. graf
Article in English | LILACS, BBO | ID: biblio-954491

ABSTRACT

Abstract Objective This study evaluated the influence of platelet-rich plasma (PRP) on the behaviour of human gingival fibroblasts (hGFs), including fibroblast proliferation, migration and colony formation. Methods PRP was obtained from the human peripheral blood of a healthy volunteer and then was diluted into platelet concentrations of 1%, 2% and 5%. The proliferation of hGFs was determined by two methods: (1) Cell-number counting with a haemocytometer method at days 1, 3, 5 and 7; (2) Colony-forming unit-fibroblast (CFU-F) assay at 2 weeks. The migration of hGFs was evaluated with scratch assay, then recorded digital images were analysed by Image-Analysis J 1.51j8 software to compare the remaining artificial wound areas between PRP groups at 0, 24 and 48 hours. Results All hGFs that were cultivated in media with 1%, 2% and 5% PRP showed their ability to proliferate and migrate. Cell numbers incubated with 1% PRP increased significantly during the first three days and peaked at day 5, tending to be similar to their proliferation in complete medium. With concentrations of 2% and 5% PRP, hGFs outgrew and peaked at day 3, which was faster than with those in medium with 1% PRP. Especially, hGFs in the group 5% PRP proliferated with higher cell numbers than those in the other remaining groups at day 3. The hGF colony number that was formed in the group 5% PRP was significantly higher than those in the groups 1% and 2% PRP. Scratch assay showed hGFs in the groups 2% and 5% PRP almost filled the artificial wound and migrated more effectively than in the group 1% PRP at 24 hours, which was significant. Conclusion In this study, perhaps the medium with 5% PRP is the dominant option, promoting the abilities of hGFs to heal wounds, because of its fast and effective impact on cell proliferation, colony formation and migration.


Subject(s)
Humans , Cell Movement/physiology , Reproducibility of Results , Cell Proliferation/physiology , Fibroblasts/drug effects , Fibroblasts/physiology , Time Factors , Cell Count , Cell Movement/drug effects , Cells, Cultured , Culture Media , Cell Proliferation/drug effects , Platelet-Rich Plasma , Gingiva/cytology
20.
J. appl. oral sci ; 26: e20160629, 2018. graf
Article in English | LILACS, BBO | ID: biblio-893696

ABSTRACT

Abstract Objective: The aim of the study was to evaluate the effects of the capping materials mineral trioxide aggregate (MTA), calcium hydroxide (CH) and BiodentineTM (BD) on stem cells from human exfoliated deciduous teeth (SHED) in vitro. Material and Methods: SHED were cultured for 1 - 7 days in medium conditioned by incubation with MTA, BD or CH (1 mg/mL), and tested for viability (MTT assay) and proliferation (SRB assay). Also, the migration of serum-starved SHED towards conditioned media was assayed in companion plates, with 8 μm-pore-sized membranes, for 24 h. Gene expression of dentin matrix protein-1 (DMP-1) was evaluated by reverse-transcription polymerase chain reaction. Regular culture medium with 10% FBS (without conditioning) and culture medium supplemented with 20% FBS were used as controls. Results: MTA, CH and BD conditioned media maintained cell viability and allowed continuous SHED proliferation, with CH conditioned medium causing the highest positive effect on proliferation at the end of the treatment period (compared with BD and MTA) (p<0.05). In contrast, we observed increased SHED migration towards BD and MTA conditioned media (compared with CH) (p<0.05). A greater amount of DMP-1 gene was expressed in MTA group compared with the other groups from day 7 up to day 21. Conclusion: Our results show that the three capping materials are biocompatible, maintain viability and stimulate proliferation, migration and differentiation in a key dental stem cell population.


Subject(s)
Humans , Oxides/pharmacology , Stem Cells/drug effects , Tooth, Deciduous/cytology , Calcium Hydroxide/pharmacology , Silicates/pharmacology , Calcium Compounds/pharmacology , Aluminum Compounds/pharmacology , Pulp Capping and Pulpectomy Agents/pharmacology , Phosphoproteins/analysis , Stem Cells/physiology , Time Factors , Tooth, Deciduous/drug effects , Materials Testing , Cell Differentiation/drug effects , Cell Movement/drug effects , Cell Survival/drug effects , Cells, Cultured , Reproducibility of Results , Analysis of Variance , Extracellular Matrix Proteins/analysis , Reverse Transcriptase Polymerase Chain Reaction , Dental Pulp Capping/methods , Cell Proliferation/drug effects , Drug Combinations , Glyceraldehyde-3-Phosphate Dehydrogenases/drug effects
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