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  1 / 1528 MEDLINE  
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[PMID]:28458357
[Au] Autor:Wang R; Zheng QX; Wang W; Feng L; Li HJ; Huai QY
[Ad] Endereço:Marine College, Shandong University.
[Ti] Título:Design and Synthesis of New Anticancer Glycyrrhetinic Acids and Oleanolic Acids.
[So] Source:Biol Pharm Bull;40(5):703-710, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:A series of new glycyrrhetinic acids and oleanolic acids has been designed and synthesized based on the principles of combinatorial chemical synthesis. Their anticancer activities were further studied by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method with hepatocellular carcinoma (Hep-G2), breast cancer (MCF-7) cell lines and a normal hepatic cell (LO2). Cytotoxicity tests (in vitro) indicated that compound 6a showed the highest cytotoxicity with the lowest IC values of 23.34 µM on Hep-G2 cells, 12.23 µM on MCF-7 cells, and 44.47 µM on LO2, which would widen the structural diversity of these anticancer targets and confirm the perspectives of further investigations.
[Mh] Termos MeSH primário: Antineoplásicos/síntese química
Desenho de Drogas
Ácido Glicirretínico/análogos & derivados
Ácido Glicirretínico/síntese química
Ácido Oleanólico/análogos & derivados
Ácido Oleanólico/síntese química
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Ácido Glicirretínico/química
Células Hep G2
Seres Humanos
Células MCF-7
Ácido Oleanólico/química
Relação Estrutura-Atividade
Sais de Tetrazólio
Tiazóis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Tetrazolium Salts); 0 (Thiazoles); 6SMK8R7TGJ (Oleanolic Acid); EUY85H477I (thiazolyl blue); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b17-00016


  2 / 1528 MEDLINE  
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[PMID]:28369869
[Au] Autor:Talbot J; Brion R; Lamora A; Mullard M; Morice S; Heymann D; Verrecchia F
[Ad] Endereço:INSERM, UMR 957, Nantes, France.
[Ti] Título:Connexin43 intercellular communication drives the early differentiation of human bone marrow stromal cells into osteoblasts.
[So] Source:J Cell Physiol;233(2):946-957, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although it has been demonstrated that human bone marrow stromal cells (hBMSCs) express the ubiquitous connexin43 (Cx43) and form functional gap junctions, their role in the early differentiation of hBMSCs into osteoblasts remains poorly documented. Using in vitro assays, we show that Cx43 expression and gap junctional intercellular communication (GJIC) are increased during the differentiation of hBMSCs into osteoblasts, both at the protein and mRNA levels. Two independent procedures to reduce GJIC, a pharmacological approach with GJIC inhibitors (18α-glycyrrhetinic acid and Gap27 peptide) and a molecular approach using small interfering RNA against Cx43, demonstrated that the presence of Cx43 and functional junctional channels are essential to the ability of hBMSCs to differentiate into osteoblasts in vitro. In addition, a reduced GJIC decreases the expression of Runx2, the major transcription factor implicated in the control of osteoblast commitment and early differentiation of hBMSCs into osteoblasts, suggesting that GJIC mediated by Cx43 is implicated in this process. Together our results demonstrate that GJIC mediated by the Cx43 channels plays a central role throughout the differentiation of hBMSC into osteoblasts, from the early stages to the process of mineralization.
[Mh] Termos MeSH primário: Células da Medula Óssea/metabolismo
Comunicação Celular
Diferenciação Celular
Conexina 43/metabolismo
Junções Comunicantes/metabolismo
Osteoblastos/metabolismo
Osteogênese
Células Estromais/metabolismo
[Mh] Termos MeSH secundário: Células da Medula Óssea/efeitos dos fármacos
Comunicação Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Conexina 43/genética
Conexinas/farmacologia
Junções Comunicantes/efeitos dos fármacos
Ácido Glicirretínico/análogos & derivados
Ácido Glicirretínico/farmacologia
Seres Humanos
Osteoblastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Interferência de RNA
Transdução de Sinais
Células Estromais/efeitos dos fármacos
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (GJA1 protein, human); 0 (gap 27 peptide); 1449-05-4 (18alpha-glycyrrhetinic acid); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25938


  3 / 1528 MEDLINE  
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[PMID]:28838831
[Au] Autor:Li K; Ma T; Cai J; Huang M; Guo H; Zhou D; Luan S; Yang J; Liu D; Jing Y; Zhao L
[Ad] Endereço:Key Laboratory of Structure-Based Drugs Design & Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, China.
[Ti] Título:Conjugates of 18ß-glycyrrhetinic acid derivatives with 3-(1H-benzo[d]imidazol-2-yl)propanoic acid as Pin1 inhibitors displaying anti-prostate cancer ability.
[So] Source:Bioorg Med Chem;25(20):5441-5451, 2017 Oct 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Twenty-six conjugates of 18ß-glycyrrhetinic acid derivatives with 3-(1H-benzo[d]imidazol-2-yl)propanoic acid were designed and synthesized as Pin1 inhibitors. Most of these semi-synthetic compounds showed improved Pin1 inhibitory activity and anti-proliferative effects against prostate cancer cells as compared to 3-(1H-benzo[d]imidazol-2-yl)propanoic acid and GA. Compounds 10a and 12i were the most potent to inhibit growth of prostate cancer PC-3 with GI values of 7.80µM and 3.52µM, respectively. The enzyme inhibition ratio of nine compounds at 10µM was over 90%. Structure-activity relationships indicated that both appropriate structure at ring C of GA and suitable length of linker between GA skeleton and benzimidazole moiety had significant impact on improving activity. Western blot assay revealed that 10a decreased the level of cell cycle regulating protein cyclin D1. Thus, these compounds might represent a novel anti-proliferative agent working through Pin1 inhibition.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Inibidores Enzimáticos/farmacologia
Ácido Glicirretínico/análogos & derivados
Imidazóis/farmacologia
Peptidilprolil Isomerase de Interação com NIMA/antagonistas & inibidores
Propionatos/farmacologia
Neoplasias da Próstata/tratamento farmacológico
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Ácido Glicirretínico/química
Ácido Glicirretínico/farmacologia
Seres Humanos
Imidazóis/química
Masculino
Conformação Molecular
Peptidilprolil Isomerase de Interação com NIMA/metabolismo
Propionatos/química
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-(1H-benzo(d)imidazol-2-yl)propanoic acid); 0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); 0 (Imidazoles); 0 (NIMA-Interacting Peptidylprolyl Isomerase); 0 (Propionates); 1449-05-4 (18alpha-glycyrrhetinic acid); EC 5.2.1.8 (PIN1 protein, human); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


  4 / 1528 MEDLINE  
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[PMID]:28813533
[Au] Autor:Hung CF; Hsiao CY; Hsieh WH; Li HJ; Tsai YJ; Lin CN; Chang HH; Wu NL
[Ad] Endereço:School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
[Ti] Título:18ß-glycyrrhetinic acid derivative promotes proliferation, migration and aquaporin-3 expression in human dermal fibroblasts.
[So] Source:PLoS One;12(8):e0182981, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Licorice (Glycyrrhiza) species have been widely used as a traditional medicine and a natural sweetener in foods. The 18ß-glycyrrhetinic acid (18ß-GA) is a bioactive compound in licorice that exhibits potential anti-cancer, anti-inflammatory, and anti-microbial activities. Many synthesized derivatives of 18ß-GA have been reported to be cytotoxic and suggested for the treatment of malignant diseases. In this study, we explored the possible pharmacological roles of an 18ß-GA derivative in skin biology using primary human dermal fibroblasts and HaCaT keratinocytes as cell models. We found that this 18ß-GA derivative did not cause cell death, but significantly enhanced the proliferation of dermal fibroblasts and HaCaT keratinocytes. A scratch wound healing assay revealed that the 18ß-GA derivative promoted the migration of fibroblasts. Due to the important role of aquaporin-3 in cell migration and proliferation, we also investigated the expression of aquaporin-3 and found this compound up-regulated the expression of aquaporin-3 in dermal fibroblasts and HaCaT keratinocytes. In dermal fibroblasts, the 18ß-GA derivative induced the phosphorylation of Akt, ERK, and p38. The inhibitor of Akt predominantly suppressed the 18ß-GA derivative-induced expression of aquaporin-3. Collectively, this compound had a positive effect on the proliferation, migration, and aquaporin-3 expression of skin cells, implying its potential role in the treatment of skin diseases characterized by impaired wound healing or dermal defects.
[Mh] Termos MeSH primário: Aquaporina 3/genética
Derme/citologia
Derme/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Ácido Glicirretínico/análogos & derivados
[Mh] Termos MeSH secundário: Aquaporina 3/metabolismo
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ácido Glicirretínico/química
Ácido Glicirretínico/farmacologia
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
1449-05-4 (18alpha-glycyrrhetinic acid); 158801-98-0 (Aquaporin 3); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182981


  5 / 1528 MEDLINE  
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[PMID]:28803048
[Au] Autor:Li B; Cai S; Yang YA; Chen SC; Chen R; Shi JB; Liu XH; Tang WJ
[Ad] Endereço:School of Pharmacy, Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, Anhui Medical University, Hefei 230032, China.
[Ti] Título:Novel unsaturated glycyrrhetic acids derivatives: Design, synthesis and anti-inflammatory activity.
[So] Source:Eur J Med Chem;139:337-348, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:To develop novel anti-inflammatory agents, a series of unsaturated glycyrrhetic acids were designed, synthesized and evaluated for anti-inflammatory activity using RAW264.7 cells. The structure-activity relationship (SAR) of NO inhibitory activity was analyzed. α,ß-Unsaturated glycyrrhetic acids showed better activity, among them, compounds 6k and 6l with piperazine unit exhibited the most potent nitric oxide (NO) and interleukin-6 (IL-6) inhibitory activity (IC = 13.3 and 15.5 µM respectively). Furthermore, compound 6k could also significantly suppress LPS-induced iNOS and COX-2 expression and IL-6 production through MAPKs and NF-kB signaling pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Desenho de Drogas
Ácido Glicirretínico/farmacologia
Interleucina-6/antagonistas & inibidores
Óxido Nítrico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/síntese química
Anti-Inflamatórios não Esteroides/química
Sobrevivência Celular/efeitos dos fármacos
Ciclo-Oxigenase 2/metabolismo
Relação Dose-Resposta a Droga
Ácido Glicirretínico/síntese química
Ácido Glicirretínico/química
Interleucina-6/biossíntese
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Camundongos
Estrutura Molecular
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/metabolismo
Células RAW 264.7
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Interleukin-6); 0 (Lipopolysaccharides); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 2); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


  6 / 1528 MEDLINE  
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[PMID]:28797028
[Au] Autor:Cirillo N; Morgan DJ; Pedicillo MC; Celentano A; Lo Muzio L; McCullough MJ; Prime SS
[Ad] Endereço:Melbourne Dental School, The University of Melbourne, 720 Swanston Street, Carlton, Melbourne, VIC 3053, Australia.
[Ti] Título:Characterisation of the cancer-associated glucocorticoid system: key role of 11ß-hydroxysteroid dehydrogenase type 2.
[So] Source:Br J Cancer;117(7):984-993, 2017 Sep 26.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent studies have shown that production of cortisol not only takes place in several non-adrenal peripheral tissues such as epithelial cells but, also, the local inter-conversion between cortisone and cortisol is regulated by the 11ß-hydroxysteroid dehydrogenases (11ß-HSDs). However, little is known about the activity of this non-adrenal glucocorticoid system in cancers. METHODS: The presence of a functioning glucocorticoid system was assessed in human skin squamous cell carcinoma (SCC) and melanoma and further, in 16 epithelial cell lines from 8 different tissue types using ELISA, western blotting and immunofluorescence. 11ß-HSD2 was inhibited both pharmacologically and by siRNA technology. Naïve CD8 T cells were used to test the paracrine effects of cancer-derived cortisol on the immune system in vitro. Functional assays included cell-cell adhesion and cohesion in two- and three-dimensional models. Immunohistochemical data of 11ß-HSD expression were generated using tissue microarrays of 40 cases of human SCCs as well as a database featuring 315 cancer cases from 15 different tissues. RESULTS: We show that cortisol production is a common feature of malignant cells and has paracrine functions. Cortisol production correlated with the magnitude of glucocorticoid receptor (GR)-dependent inhibition of tumour-specific CD8 T cells in vitro. 11ß-HSDs were detectable in human skin SCCs and melanoma. Analyses of publicly available protein expression data of 11ß-HSDs demonstrated that 11ß-HSD1 and -HSD2 were dysregulated in the majority (73%) of malignancies. Pharmacological manipulation of 11ß-HSD2 activity by 18ß-glycyrrhetinic acid (GA) and silencing by specific siRNAs modulated the bioavailability of cortisol. Cortisol also acted in an autocrine manner and promoted cell invasion in vitro and cell-cell adhesion and cohesion in two- and three-dimensional models. Immunohistochemical analyses using tissue microarrays showed that expression of 11ß-HSD2 was significantly reduced in human SCCs of the skin. CONCLUSIONS: The results demonstrate evidence of a cancer-associated glucocorticoid system and show for the first time, the functional significance of cancer-derived cortisol in tumour progression.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 2/metabolismo
Carcinoma de Células Escamosas/enzimologia
Células Epiteliais/enzimologia
Hidrocortisona/metabolismo
Melanoma/enzimologia
Neoplasias Cutâneas/enzimologia
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/metabolismo
11-beta-Hidroxiesteroide Desidrogenase Tipo 2/análise
11-beta-Hidroxiesteroide Desidrogenase Tipo 2/antagonistas & inibidores
11-beta-Hidroxiesteroide Desidrogenase Tipo 2/genética
Hormônio Adrenocorticotrópico/farmacologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Carcinoma de Células Escamosas/química
Adesão Celular
Proliferação Celular/efeitos dos fármacos
Cortisona/farmacologia
Meios de Cultivo Condicionados/farmacologia
Regulação para Baixo
Inativação Gênica
Ácido Glicirretínico/análogos & derivados
Ácido Glicirretínico/farmacologia
Células HT29
Seres Humanos
Hidrocortisona/imunologia
Hidrocortisona/farmacologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Células MCF-7
Melanoma/química
Comunicação Parácrina
Receptores de Glucocorticoides/imunologia
Receptores de Glucocorticoides/metabolismo
Neoplasias Cutâneas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Receptors, Glucocorticoid); 1449-05-4 (18alpha-glycyrrhetinic acid); 9002-60-2 (Adrenocorticotropic Hormone); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 1); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 2); P540XA09DR (Glycyrrhetinic Acid); V27W9254FZ (Cortisone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.243


  7 / 1528 MEDLINE  
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[PMID]:28768154
[Au] Autor:Sun YQ; Dai CM; Zheng Y; Shi SD; Hu HY; Chen DW
[Ad] Endereço:School of Pharmacy, Jinzhou Medical University, Jinzhou, PR China; School of Pharmacy, Shenyang Pharmaceutical University, Shenyang, PR China.
[Ti] Título:Binding effect of fluorescence labeled glycyrrhetinic acid with GA receptors in hepatocellular carcinoma cells.
[So] Source:Life Sci;188:186-191, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Glycyrrhetinic acid (GA) is a natural active component from licorice, which is broadly used in traditional Chinese medicine. Lots of glycyrrhetinic acid receptors (GA-R) are proved to locate on the surface of liver cells. Many reports about the hepatocellular carcinoma (HCC) treatment were dependent on GA modified carriers. However, the reality of GA-R in HCC cells was not clear. In this paper, 18ß-glycyrrhetinic acid (18ß-GA) was labeled with fluorescence (FITC) by chemical synthesis. Together with the binding effect of fluorescence labeled glycyrrhetinic acid (FITC-GA), the competitive action of 18ß-GA with GA-R was investigated in HCC cells. The results showed that in HepG2 cells, 18ß-GA and FITC-GA presented similar cytotoxicity. The specific binding saturation of GA showed the dissociation constant (K ) was 7.457±2.122pmol/L and the maximum binding counts (B ) was 2.385±0.175pmol/2.5×10 cells, respectively. FITC-GA bound to cytomembrane specifically and 18ß-GA competed to bind the sites significantly in HepG2 cells. Therefore, there is binding effect between fluorescence labeled GA and GA-R. The GA-R on HCC cells is confirmed as expected, which provides a useful reference of active target modified by GA and a novel approach for receptors and ligands study.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Ácido Glicirretínico/análogos & derivados
Ligantes
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Ligação Competitiva
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Fluoresceína-5-Isotiocianato/química
Fluoresceína-5-Isotiocianato/metabolismo
Fluoresceína-5-Isotiocianato/farmacologia
Ácido Glicirretínico/química
Ácido Glicirretínico/metabolismo
Ácido Glicirretínico/farmacologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 1449-05-4 (18alpha-glycyrrhetinic acid); I223NX31W9 (Fluorescein-5-isothiocyanate); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE


  8 / 1528 MEDLINE  
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[PMID]:28685526
[Au] Autor:Chen D; Bellussi LM; Cocca S; Wang J; Passali GC; Hao X; Chen L; Passali D
[Ad] Endereço:Department of Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, China.
[Ti] Título:Glycyrrhetinic acid suppressed hmgb1 release by up-regulation of Sirt6 in nasal inflammation.
[So] Source:J Biol Regul Homeost Agents;31(2):269-277, 2017 Apr-Jun.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:To extend our understanding of previous studies on the pathogenesis and mechanism of high mobility group box 1 (HMGB1) in chronic rhinosinusitis with nasal polyps (CRSwNP), here we show that Sirtuin 6 (Sirt6), one of the Sirtuin family members which are widely studied in aging, DNA repair, metabolism, inflammation and cancer, was expressed in normal nasal mucosa using immunohistochemical staining and Western blot assay. Sirt6 expression levels were decreased in CRSwNP tissue. Sirt6 expression levels were modulated by small interfering RNA transfection in human nasal epithelial cells (HNE). We found that depletion of Sirt6 suppressed the number of human nasal epithelial cell cilia, and dramatically induced HMGB1 translocation from nucleus to cytoplasm in the HNE cells. Glycyrrhizic acid (GA) and glycyrrhetinic acid (GTA) are specific chemical compounds that may be isolated from the licorice plant. GTA has been shown to have anti-inflammatory and anti-allergic activity: it binds selectively to HMGB1 protein released extra-cellularly and inhibits its cytokine activities through a scavenger mechanism on the protein accumulation. In an in vitro study we used the 18-ß-stereoisomer of GTA to enhance Sirt6 expression levels, inhibiting through this mechanism the translocation of HMGB1 protein from nucleus and reversing its extracellular accumulation stimulated by lipopolysaccharides. These findings reveal a previously unknown role for nasal mucosa steady-state conditions in the control of Sirt6 activity, and provide evidence for a relationship between HMGB1 and Sirt6 in CRSwNP, and promising benefits of glycyrrhetinic acid for CRSwNP patients.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Ácido Glicirretínico/farmacologia
Proteína HMGB1/secreção
Pólipos Nasais/metabolismo
Rinite/metabolismo
Sinusite/metabolismo
Sirtuínas/biossíntese
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doença Crônica
Feminino
Seres Humanos
Inflamação/metabolismo
Inflamação/patologia
Masculino
Pólipos Nasais/patologia
Rinite/patologia
Sinusite/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HMGB1 Protein); 0 (HMGB1 protein, human); EC 3.5.1.- (SIRT6 protein, human); EC 3.5.1.- (Sirtuins); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


  9 / 1528 MEDLINE  
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[PMID]:28652738
[Au] Autor:Lv Y; Li J; Chen H; Bai Y; Zhang L
[Ad] Endereço:Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Research Center for Pharmaceutical Engineering, College of Pharmacy, Chongqing Medical University, Chongqing, China.
[Ti] Título:Glycyrrhetinic acid-functionalized mesoporous silica nanoparticles as hepatocellular carcinoma-targeted drug carrier.
[So] Source:Int J Nanomedicine;12:4361-4370, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:In this study, a glycyrrhetinic acid-functionalized mesoporous silica nanoparticle (MSN-GA) was prepared for active tumor targeting. MSN-GA exhibited satisfactory loading capacity for insoluble drugs, uniform size distribution, and specific tumor cell targeting. Glycyrrhetinic acid, a hepatocellular carcinoma-targeting group, was covalently decorated on the surface of MSN via an amido bond. The successful synthesis of MSN-GA was validated by the results of Fourier transform infrared spectroscopy, transmission electron microscopy (TEM), and zeta potential measurement. TEM images revealed the spherical morphology and uniform size distribution of the naked MSN and MSN-GA. Curcumin (CUR), an insoluble model drug, was loaded into MSN-GA (denoted as MSN-GA-CUR) with a high-loading capacity (8.78%±1.24%). The results of the in vitro cellular experiment demonstrated that MSN-GA-CUR significantly enhanced cytotoxicity and cellular uptake toward hepatocellular carcinoma (HepG2) cells via a specific GA receptor-mediated endocytosis mechanism. The results of this study provide a promising nanoplatform for the targeting of hepatocellular carcinoma.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Portadores de Fármacos/química
Ácido Glicirretínico/farmacologia
Nanopartículas/química
[Mh] Termos MeSH secundário: Antineoplásicos/química
Antineoplásicos/farmacologia
Carcinoma Hepatocelular/tratamento farmacológico
Curcumina/administração & dosagem
Curcumina/química
Curcumina/farmacologia
Portadores de Fármacos/administração & dosagem
Difusão Dinâmica da Luz
Ácido Glicirretínico/administração & dosagem
Ácido Glicirretínico/química
Células Hep G2/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Microscopia Eletrônica de Transmissão
Nanopartículas/administração & dosagem
Dióxido de Silício/química
Espectroscopia de Infravermelho com Transformada de Fourier
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Carriers); 7631-86-9 (Silicon Dioxide); IT942ZTH98 (Curcumin); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S135626


  10 / 1528 MEDLINE  
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[PMID]:28638869
[Au] Autor:Zhang Y; Yu L; Jin W; Fan H; Li M; Zhou T; Wan H; Yang J
[Ad] Endereço:Zhejiang Chinese Medical University, Hangzhou 310053, P.R. China.
[Ti] Título:REDUCING TOXICITY AND INCREASING EFFICIENCY: ACONITINE WITH LIQUIRITIN AND GLYCYRRHETINIC ACID REGULATE CALCIUM REGULATORY PROTEINS IN RAT MYOCARDIAL CELL.
[So] Source:Afr J Tradit Complement Altern Med;14(4):69-79, 2017.
[Is] ISSN:2505-0044
[Cp] País de publicação:Nigeria
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Compatibility of and is known to treat heart diseases such as heart failure and cardiac arrhythmias. This work answers the question that whether the active components (Aconitine, Liquiritin and Glycyrrhetinic Acid) of and could result in regulating intracellular calcium homeostasis and calcium cycling, and thereby verifies the therapeutic material basis. MATERIALS AND METHODS: The myocardial cells were divided into twelve groups randomly as control group, Aconitine group, nine different dose groups that orthogonal combined with Aconitine, Liquiritin and Glycyrrhetinic Acid, and Verapamil group. The myocardial cellular survival rate and morphology were assessed. The expression of calcium regulation protein(RyR2, NCX1, DHPR-a1) in the myocardial cell by Western-blotting. RESULTS: The results exhibited that Aconitine (120 uM) significantly damaged on myocardial cell, decreased the survival rate and expression of Na /Ca exchangers (NCX1) and dihydropteridine reducta-α1 (DHPR-a1), and increased the expression of ryanodine receptor type2 (RyR2) obviously. The compatibility groups (Aconitine, Liquiritin and Glycyrrhetinic Acid) all could against the damage on the myocardial cell by Aconitine at different levels. CONCLUSION: Aconitine with Liquiritin and Glycyrrhetinic Acid may regulate the expression of calcium-regulated proteins to protect myocardial cells from damage.
[Mh] Termos MeSH primário: Aconitina/farmacologia
Aconitum/química
Cálcio/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Flavanonas/farmacologia
Glucosídeos/farmacologia
Ácido Glicirretínico/farmacologia
Glycyrrhiza/química
Miócitos Cardíacos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Miócitos Cardíacos/metabolismo
Ratos
Canal de Liberação de Cálcio do Receptor de Rianodina/genética
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Trocador de Sódio e Cálcio/genética
Trocador de Sódio e Cálcio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Flavanones); 0 (Glucosides); 0 (RyR2 protein, rat); 0 (Ryanodine Receptor Calcium Release Channel); 0 (Sodium-Calcium Exchanger); 0 (sodium-calcium exchanger 1); P540XA09DR (Glycyrrhetinic Acid); SY7Q814VUP (Calcium); T0O79T74CD (liquiritin); X8YN71D5WC (Aconitine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.21010/ajtcam.v14i4.9



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