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[PMID]:28460437
[Au] Autor:Li C; Zeng M; Chi H; Shen J; Ng TB; Jin G; Lu D; Fan X; Xiong B; Xiao Z; Sha O
[Ad] Endereço:Department of Anatomy, Histology and Developmental Biology, School of Basic Medical Sciences, Shenzhen University Health Science Centre, Shenzhen, Guangdong, China.
[Ti] Título:Trichosanthin increases Granzyme B penetration into tumor cells by upregulation of CI-MPR on the cell surface.
[So] Source:Oncotarget;8(16):26460-26470, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trichosanthin is a plant toxin belonging to the family of ribosome-inactivating proteins. It has various biological and pharmacological activities, including anti-tumor and immunoregulatory effects. In this study, we explored the potential medicinal applications of trichosanthin in cancer immunotherapy. We found that trichosanthin and cation-independent mannose-6-phosphate receptor competitively bind to the Golgi-localized, γ-ear containing and Arf-binding proteins. It in turn promotes the translocation of cation-independent mannose-6-phosphate receptor from the cytosol to the plasma membrane, which is a receptor of Granzyme B. The upregulation of this receptor on the tumor cell surface increased the cell permeability to Granzyme B, and the latter is one of the major factors of cytotoxic T lymphocyte-mediated tumor cell apoptosis. These results suggest a novel potential application of trichosanthin and shed light on its anti-tumor immunotherapy.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Granzimas/metabolismo
Receptor IGF Tipo 2/metabolismo
Tricosantina/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Apoptose
Linhagem Celular Tumoral
Permeabilidade da Membrana Celular
Modelos Animais de Doenças
Seres Humanos
Masculino
Camundongos
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Tricosantina/química
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, IGF Type 2); 60318-52-7 (Trichosanthin); EC 3.4.21.- (GZMB protein, human); EC 3.4.21.- (Granzymes)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15518


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[PMID]:29185359
[Au] Autor:Hu J; Pang WS; Han J; Zhang K; Zhang JZ; Chen LD
[Ad] Endereço:a Fujian Academy of Traditional Chinese Medicine , Fuzhou , PR China.
[Ti] Título:Gualou Guizhi decoction reverses brain damage with cerebral ischemic stroke, multi-component directed multi-target to screen calcium-overload inhibitors using combination of molecular docking and protein-protein docking.
[So] Source:J Enzyme Inhib Med Chem;33(1):115-125, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Stroke is a disease of the leading causes of mortality and disability across the world, but the benefits of drugs curative effects look less compelling, intracellular calcium overload is considered to be a key pathologic factor for ischemic stroke. Gualou Guizhi decoction (GLGZD), a classical Chinese medicine compound prescription, it has been used to human clinical therapy of sequela of cerebral ischemia stroke for 10 years. This work investigated the GLGZD improved prescription against intracellular calcium overload could decreased the concentration of [Ca ] in cortex and striatum neurone of MCAO rats. GLGZD contains Trichosanthin and various small molecular that they are the potential active ingredients directed against NR2A, NR2B, FKBP12 and Calnodulin target proteins/enzyme have been screened by computer simulation. "Multicomponent systems" is capable to create pharmacological superposition effects. The Chinese medicine compound prescriptions could be considered as promising sources of candidates for discovery new agents.
[Mh] Termos MeSH primário: Isquemia Encefálica/tratamento farmacológico
Cálcio/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Simulação de Acoplamento Molecular
Bibliotecas de Moléculas Pequenas/farmacologia
Acidente Vascular Cerebral/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Oral
Animais
Relação Dose-Resposta a Droga
Medicamentos de Ervas Chinesas/administração & dosagem
Medicamentos de Ervas Chinesas/química
Ligação Proteica/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Bibliotecas de Moléculas Pequenas/administração & dosagem
Bibliotecas de Moléculas Pequenas/química
Relação Estrutura-Atividade
Proteína 1A de Ligação a Tacrolimo/antagonistas & inibidores
Proteína 1A de Ligação a Tacrolimo/metabolismo
Tricosantina/administração & dosagem
Tricosantina/química
Tricosantina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (N-methyl D-aspartate receptor subtype 2A); 0 (NR2B NMDA receptor); 0 (Receptors, N-Methyl-D-Aspartate); 0 (Small Molecule Libraries); 0 (guizhi decoction); 60318-52-7 (Trichosanthin); EC 5.2.1.- (Tacrolimus Binding Protein 1A); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1396457


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[PMID]:27714558
[Au] Autor:Lin B; Yang XZ; Cao XW; Zhang TZ; Wang FJ; Zhao J
[Ad] Endereço:State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Road, Shanghai, 200237, China.
[Ti] Título:A novel trichosanthin fusion protein with increased cytotoxicity to tumor cells.
[So] Source:Biotechnol Lett;39(1):71-78, 2017 Jan.
[Is] ISSN:1573-6776
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the anti-tumor effects of trichosanthin after fusion with a cell penetrating peptide, heparin-binding peptide (HBP), derived from human heparin-binding EGF-like growth factor (HB-EGF). RESULTS: The fusion protein of trichosanthin-HBP was expressed in Escherichia coli BL21 and purified by Ni-NTA affinity chromatography. The HBP domain had no influence on the topological inactivation activity and N-glycosidase activity of trichosanthin. Trichosanthin-HBP significantly inhibited the growth of tested cancer cells which are impervious to trichosanthin. Tumor cell apoptosis and both the mitochondrial- and death receptor-mediated apoptotic signaling pathways induced by trichosanthin-HBP were more significant than those induced by trichosanthin in HeLa cells. CONCLUSION: HBP is an efficient intracellular delivery vehicle for trichosanthin and makes trichosanthin-HBP become a promising agent for cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/metabolismo
Antineoplásicos/farmacologia
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/química
Peptídeos/metabolismo
Peptídeos/farmacologia
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes de Fusão/farmacologia
Tricosantina/metabolismo
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Células HeLa
Seres Humanos
Peptídeos/genética
Proteínas Recombinantes de Fusão/genética
Tricosantina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Heparin-binding EGF-like Growth Factor); 0 (Peptides); 0 (Recombinant Fusion Proteins); 60318-52-7 (Trichosanthin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161008
[St] Status:MEDLINE
[do] DOI:10.1007/s10529-016-2222-0


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[PMID]:27754366
[Au] Autor:Shi WW; Tang YS; Sze SY; Zhu ZN; Wong KB; Shaw PC
[Ad] Endereço:Centre for Protein Science and Crystallography, School of Life Sciences, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China. Shiww@cuhk.edu.hk.
[Ti] Título:Crystal Structure of Ribosome-Inactivating Protein Ricin A Chain in Complex with the C-Terminal Peptide of the Ribosomal Stalk Protein P2.
[So] Source:Toxins (Basel);8(10), 2016 10 13.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Ricin is a type 2 ribosome-inactivating protein (RIP), containing a catalytic A chain and a lectin-like B chain. It inhibits protein synthesis by depurinating the N-glycosidic bond at α-sarcin/ricin loop (SRL) of the 28S rRNA, which thereby prevents the binding of elongation factors to the GTPase activation center of the ribosome. Here, we present the 1.6 Å crystal structure of Ricin A chain (RTA) complexed to the C-terminal peptide of the ribosomal stalk protein P2, which plays a crucial role in specific recognition of elongation factors and recruitment of eukaryote-specific RIPs to the ribosomes. Our structure reveals that the C-terminal GFGLFD motif of P2 peptide is inserted into a hydrophobic pocket of RTA, while the interaction assays demonstrate the structurally untraced SDDDM motif of P2 peptide contributes to the interaction with RTA. This interaction mode of RTA and P protein is in contrast to that with trichosanthin (TCS), Shiga-toxin (Stx) and the active form of maize RIP (MOD), implying the flexibility of the P2 peptide-RIP interaction, for the latter to gain access to ribosome.
[Mh] Termos MeSH primário: Fosfoproteínas/química
Proteínas Ribossômicas/química
Ricina/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Clonagem Molecular
Escherichia coli/genética
Peptídeos/química
Conformação Proteica
Ricina/genética
Toxina Shiga/química
Tricosantina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peptides); 0 (Phosphoproteins); 0 (Ribosomal Proteins); 0 (phosphoprotein P2, ribosomal); 60318-52-7 (Trichosanthin); 75757-64-1 (Shiga Toxin); 9009-86-3 (Ricin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161019
[St] Status:MEDLINE


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[PMID]:27050721
[Au] Autor:Lu YZ; Li PF; Li YZ; Luo F; Guo C; Lin B; Cao XW; Zhao J; Wang FJ
[Ad] Endereço:State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, China.
[Ti] Título:Enhanced anti-tumor activity of trichosanthin after combination with a human-derived cell-penetrating peptide, and a possible mechanism of activity.
[So] Source:Fitoterapia;112:183-90, 2016 Jul.
[Is] ISSN:1873-6971
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Trichosanthin (TCS), a type I ribosome-inactivating protein (RIP-I) and renowned Chinese traditional medicine, displays a broad spectrum of biological and pharmacological properties. Particularly, its anti-tumor activity has received a great deal of attention. However, the cellular mechanism for TCS uptake varies with different tumor cell lines, leading to discrepancies in its reported ability to penetrate cells. In this study, HBD, a human derived cell-penetrating peptide (CPP), was used to improve the delivery of TCS into several types of tumor cells, including HeLa cells. Recombinant TCS (rTCS) with or without the fused HBD peptide was expressed in Escherichia coli cells and successfully purified by Ni-NTA affinity chromatography. The cellular uptake efficiency of FITC-labelled-rTCS-HBD was observed in HeLa cells and compared with the uptake efficiency of non-HBD conjugated rTCS under the same conditions using laser confocal microscopy. Moreover, the IC50 value of rTCS-HBD in the tested tumor cells was much lower than that of rTCS, indicating that HBD could efficiently deliver the rTCS into tumor cells. When compared with rTCS, rTCS-HBD induced higher rates of apoptosis in HeLa cells as analyzed by flow cytometry. Furthermore, the apoptotic events observed in HeLa cells incubated with HBD-fused rTCS included activation of Caspase-9, decrease in the Bcl-2/Bax ratio, and cleavage of PARP. These results strongly suggest the participation of mitochondria in apoptosis. This report illustrates one possible method for achieving the efficient transport of TCS into cells using a CPP as a vector, and increases the likelihood that TCS can be used in the clinic.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Peptídeos Penetradores de Células/química
Portadores de Fármacos/química
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Apoptose
Linhagem Celular Tumoral
Células HeLa
Seres Humanos
Proteínas Recombinantes de Fusão/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Cell-Penetrating Peptides); 0 (Drug Carriers); 0 (Recombinant Fusion Proteins); 60318-52-7 (Trichosanthin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE


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[PMID]:27032906
[Au] Autor:Wei B; Huang Q; Huang S; Mai W; Zhong X
[Ad] Endereço:People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, Guangxi, China.
[Ti] Título:Trichosanthin-induced autophagy in gastric cancer cell MKN-45 is dependent on reactive oxygen species (ROS) and NF-κB/p53 pathway.
[So] Source:J Pharmacol Sci;131(2):77-83, 2016 Jun.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Trichosanthin (TCS), isolated from the root tuber of Trichosanthes kirilowii tubers in the Cucurbitaceae family, owns a great deal of biological and pharmacological activities including anti-virus and anti-tumor. TCS has been reported to induce cell apoptosis of a diversity of cancers, including cervical cancer, choriocarcinoma, and gastric cancer, etc. However, whether TCS would induce autophagy in gastric cancer cells was seldom investigated. In current study, human gastric cancer MKN-45 cell growth was significantly inhibited by TCS. The anti-proliferation effect of TCS was due to an increased autophagy, which was confirmed by monodansylcadervarine (MDC) staining, up-regulation of Autophagy protein 5 (Atg5), and conversion of LC3 I to LC3 II (autophagosome marker). In addition, TCS induced reactive oxygen species (ROS) in MKN-45 cells and ROS scavenger N-acetylcysteine (NAC) significantly reversed TCS-induced autophagy. Furthermore, NF-κB/p53 pathway was activated during the process of autophagy induced by TCS and the ROS generation was mediated by it in MKN-45 cells. In vivo results showed that TCS exerted significantly anti-tumor effect on MKN-45 bearing mice. Considering the clinical usage of TCS on other human diseases, these research progresses provided a new insight into cancer research and new therapeutic avenues for patients with gastric cancer.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Autofagia/efeitos dos fármacos
NF-kappa B/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Neoplasias Gástricas/metabolismo
Tricosantina/farmacologia
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Fitogênicos/uso terapêutico
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Gástricas/tratamento farmacológico
Tricosantina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (NF-kappa B); 0 (Reactive Oxygen Species); 0 (Tumor Suppressor Protein p53); 60318-52-7 (Trichosanthin); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160402
[St] Status:MEDLINE


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[PMID]:27015938
[Au] Autor:Li J; Li H; Zhang Z; Wang N; Zhang Y
[Ad] Endereço:Department of Laboratory Medicine, The Second Affiliated Hospital of Southeast University, Zhongfu Road 1-1, Nanjing, 210003, China.
[Ti] Título:The anti-cancerous activity of recombinant trichosanthin on prostate cancer cell PC3.
[So] Source:Biol Res;49:21, 2016 Mar 25.
[Is] ISSN:0717-6287
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Trichosanthin produced in the root tube of Trichosanthes kirilowii shows anti-tumor activity on a series of cancer cells including Hela, MCF-7, HL-60. But there is little information about its effect on the carcinogenesis of prostate cancer. OBJECTIVE: This work was designed to study the role of trichosanthin on prostate cancer cells PC3. MATERIALS AND METHODS: Trichosanthin was expressed in BL21 strain and purified by affinity chromatography. MTT assay was designed to determine the effect of trichosanthin on growth of PC3 cells at doses of 10, 20, 40, 60, 80, and 120 µg/ml. Then the effect of 50 µg/ml rTCS alone or combined with 2 µM IL-2 on PC3 cell proliferation was analyzed. And the mechanism of rTCS was studied by western blot. After that the in vivo effect of rTCS combined with IL-2 was explored in mice bearing PC3 xenograft tumor. RESULTS: Trichosanthin was successfully expressed in BL21 and purified by 100 mM imidazole. It was shown to inhibit proliferation of PC3 cells in a dose-dependent manner with IC50 50.6 µg/ml. When combined with cytokine IL-2, a significant synergic effect was obtained. The inhibition rate on PC3 was around 50 % in combination group while only 35.5 % in single rTCS group at 50 µg/ml. Further, the expression of full length caspase-8 and Bcl-2 decreased significantly while cleaved caspase-8 and Bax were up-regulated, which suggest that caspase-8-mediated apoptosis pathway may be activated by rTCS in PC3 cells. Moreover, our data demonstrated that tumor volume and tumor weight were significantly reduced in rTCS-treated or rTCS/IL-2-treated nude mice bearing PC3 xenograft tumor compared with control. And significant difference was also found between rTCS and rTCS/IL-2 group. CONCLUSIONS: This study demonstrates that rTCS is a potential agent with high in vitro and in vivo anti-tumor activity on PC3 cells. And rTCS combined with IL-2 is a promising strategy in treating patients with prostate cancer in future.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Neoplasias da Próstata/tratamento farmacológico
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Western Blotting
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Feminino
Formazans
Masculino
Camundongos
Neoplasias da Próstata/patologia
Proteínas Recombinantes/farmacologia
Reprodutibilidade dos Testes
Sais de Tetrazólio
Fatores de Tempo
Carga Tumoral
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Formazans); 0 (Recombinant Proteins); 0 (Tetrazolium Salts); 23305-68-2 (MTT formazan); 60318-52-7 (Trichosanthin)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160327
[St] Status:MEDLINE
[do] DOI:10.1186/s40659-016-0081-8


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[PMID]:26694804
[Au] Autor:Li Z; Yang N; Zhou L; Gu P; Wang H; Zhou Y; Zhou P; Lu L; Chou KY
[Ad] Endereço:Shanghai Institute of Immunology, Shanghai, China.
[Ti] Título:A peptide tetramer Tk-tPN induces tolerance of cardiac allografting by conversion of type 1 to type 2 immune responses via the Toll-like receptor 2 signal-promoted activation of the MCP1 gene.
[So] Source:Immunology;147(3):355-66, 2016 Mar.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The plant protein trichosanthin (Tk) and its derived peptide tetramer Tk-tPN have been shown to stimulate the type 2 immune responses for treating autoimmune disease. This work explores the possibility of using Tk-tPN as a non-toxic immunosuppressant to induce transplantation tolerance using the mechanisms by which T-cell-mediated immune responses are transferred from type 1 to type 2 through innate immunity-related pathways. Immunocytes and cytokine secretions involved in the mouse cardiac allografting model with Tk-tPN treatment were characterized. Identification of critical genes and analysis of their functions through Toll-like receptor (TLR) -initiated signalling and the possible epigenetic changes were performed. Mean survival times of the cardiac allografts were delayed from 7.7 ± 0.3 days (control) to 22.7 ± 3.9 days (P < 0.01) or 79.1 ± 19.2 days (P < 0.0001) when Tk-tPN was introduced into the recipients alone or together with rapamycin, respectively. The grafting tolerance was donor-specific. The secretion pattern of the type 1 cytokine/transcription factor (IL-2(+) IFN-γ(+) T-bet(+)), which is responsible for the acute graft rejection, was shifted to the type 2 factor (IL-4(+) IL-10(+) Gata3+), together with a selective expansion of the IL-4/IL-10-producing CD8+ CD28- regulatory T-cell subset. A TLR2-initiated high expression of chemokine gene MCP1 was detectable simultaneously. Epigenetically Tk/Tk-tPN could also acetylate the histone H3K9 of MCP1 promoter to skew the immunity towards T helper type 2 responses. Tk/Tk-tPN is therefore capable of down-regulating the type 1 response-dominant rejection of cardiac allografts by evoking type 2 immunity through the activation of a TLR2-initiated signalling pathway and MCP1 gene to expand the IL-4/IL-10-secreting CD8+ CD28- regulatory T cells. Tk-tPN could be a promising novel immunosuppressant to induce tolerance in allotransplantation.
[Mh] Termos MeSH primário: Quimiocina CCL2/imunologia
Imunossupressores/farmacologia
Linfócitos T Reguladores/imunologia
Imunologia de Transplantes/imunologia
Tolerância ao Transplante/imunologia
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Aloenxertos
Animais
Quimiocina CCL2/genética
Quimiocina CCL2/metabolismo
Modelos Animais de Doenças
Citometria de Fluxo
Regulação da Expressão Gênica/imunologia
Sobrevivência de Enxerto/efeitos dos fármacos
Transplante de Coração
Ativação Linfocitária/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Subpopulações de Linfócitos T/imunologia
Receptor 2 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Immunosuppressive Agents); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 60318-52-7 (Trichosanthin)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151224
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12569


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[PMID]:26548896
[Au] Autor:Zhu Y; Sun Y; Cai Y; Sha O; Jiang W
[Ad] Endereço:State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Sun Yat­sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
[Ti] Título:Trichosanthin reduces the viability of SU­DHL­2 cells via the activation of the extrinsic and intrinsic apoptotic pathways.
[So] Source:Mol Med Rep;13(1):403-11, 2016 Jan.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Previous studies have indicated that trichosanthin (TCS) exerts antitumor activity by inducing apoptosis in numerous tumor cell lines. However, the effects of TCS on lymphoma remain to be elucidated. The current study demonstrated that TCS inhibited the proliferation of thirteen lymphoma cell lines in a dose­dependent manner, with SU­DHL­2 cells exhibiting the greatest sensitivity to TCS. Treatment of SU­DHL­2 cells with TCS led to cell cycle arrest at the S to G2/M phase transition. Furthermore, flow cytometric analysis, Hoechst 33258 staining and western blotting indicated that TCS induced the apoptosis of SU­DHL­2 cells in a time­ and concentration­dependent manner. In addition, the activation of caspase­3 and ­7 and poly (ADP­ribose) polymerase were observed. Pharmacological pan-caspase inhibition was observed to reduce TCS­induced apoptosis. Inhibition of caspase­8 or ­9 alone was observed to partially reverse the effect of TCS on apoptosis. In conclusion, the current study indicates that TCS may induce apoptosis in SU­DHL­2 cells via the extrinsic and intrinsic pathways.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Caspases/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Eletroforese em Gel de Poliacrilamida
Seres Humanos
Linfoma/patologia
Poli(ADP-Ribose) Polimerases/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
60318-52-7 (Trichosanthin); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151110
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2015.4531


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Fotocópia
[PMID]:26413625
[Au] Autor:Wen D; Wang J; Yan H; Chen J; Xia K; Liu J; Zhang A
[Ti] Título:Effect of Radix Trichosanthis and Trichosanthin on Hepatitis B Virus in HepG2.2.15 Cells.
[So] Source:J Nanosci Nanotechnol;15(3):2094-8, 2015 Mar.
[Is] ISSN:1533-4880
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Radix Trichosanthis is a Chinese herbal medicine that has great medical value and pharmacological actions. There is already a long history of using the plant Radix Trichosanthis as treatment for hepatitis B virus in China. This research mainly focused on investigating the therapeutic effect of different extracts from Radix Trichosanthis on hepatitis B virus, on a cellular level (ex vivo). Cell survival rate of HepG2.2.15 cells was detected by MTT assay. HBsAg and HBeAg in HepG 2.2.15 cell supernatant were evaluated by enzyme linked immunosorbent assay (ELISA). Results showed that water extract from Radix Trichosanthis had a stronger inhibitive effect on expression of HBsAg and HBeAg in HepG2.2.15 cells than the alcohol extract from the same plant. Considering that the most active component of Radix Trichosanthis was in its aqueous extract and this might be related to the active component Trichosanthin. Trichosanthin was further used for related experiments to confirm this hypothesis. The results showed that Trichosanthin, in the aqueous extract from Radix Trichosanthis, is likely the main component responsible for the anti-hepatitis B viral effect.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Vírus da Hepatite B/efeitos dos fármacos
Tricosantina/farmacologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Meios de Cultivo Condicionados/metabolismo
Células Hep G2
Antígenos de Superfície da Hepatite B/metabolismo
Antígenos E da Hepatite B/metabolismo
Vírus da Hepatite B/imunologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Culture Media, Conditioned); 0 (Drugs, Chinese Herbal); 0 (Hepatitis B Surface Antigens); 0 (Hepatitis B e Antigens); 0 (radix Trichosanthis); 60318-52-7 (Trichosanthin)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150928
[Lr] Data última revisão:
150928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150929
[St] Status:MEDLINE



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