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Find video protocols related to scientific articles indexed in Pubmed.
Reversion of trichostatin A resistance via inhibition of the Wnt signaling pathway in human pancreatic cancer cells.
Oncol. Rep.
PUBLISHED: 06-16-2014
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Drug resistance is a major impediment to successful chemotherapy in pancreatic cancer (PC) patients. We investigated the effect of Wnt/?-catenin signaling inhibition by wnt-c59 on chemoresistance in a trichostatin A-resistant Panc-1 cell line (Panc-1/TSA). Panc-1/TSA cells were treated with the Wnt/??catenin signaling inhibitor wnt-c59 (10 µmol?·?l-1) and/or trichostatin A (TSA; 10 µmol?·?l-1) for 24 h. CCK-8 assay was utilized to analyze the interactive effect of TSA and wnt-c59 on induction of apoptosis of the Panc-1/TSA cells. Cell apoptosis was measured by flow cytometry. Real-time PCR and western blotting were used to assess Wnt/?-catenin signaling, epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). Real-time cell analysis (RTCA) was used to detect the cell migration ability. After wnt-c59 treatment for 24 h, relative genes and transcriptional targets of Wnt/?-catenin signaling were downregulated (P<0.05). CCK-8 assay indicated that the combination of TSA and wnt-c59 had a synergistic effect on induction of Panc-1/TSA cell apoptosis. As detected by FACS, cell apoptosis rates increased significantly (P<0.05). The results of RTCA showed that the cell indices of the control group, wnt-c59 group, TSA group and TSA+wnt-c59 combination group were 1.2842±0.0257, 1.2155±0.0282, 1.2533±0.0194 and 0.8541±0.0250, respectively. In accordance, MMP-9 protein in the wnt-c59 treatment groups was decreased compared to the non-wnt-c59 treatment groups. Meanwhile, E-cadherin protein was upregulated and vimentin protein was downregulated, both of which are characteristic markers of EMT. Chemoresistant gene MDR1 and P-glycoprotein (P-gp) in the wnt-c59 treatment groups had a reduced expression compared to the non-wnt-c59 treatment groups. This study revealed that TSA sensitivity, migration ability, and the EMT phenotype in Panc-1/TSA cells were reversed following Wnt/?-catenin signaling inhibition.
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Solanine induces mitochondria-mediated apoptosis in human pancreatic cancer cells.
Biomed Res Int
PUBLISHED: 02-19-2014
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Steroid alkaloids have been suggested as potential anticancer compounds. However, the underlying mechanisms of how steroid alkaloids inhibit the tumor growth are largely unknown. Here, we reported that solanine, a substance of steroid alkaloids, has a positive effect on the inhibition of pancreatic cancer cell growth in vitro and in vivo. In pancreatic cancer cells and nu/nu nude mice model, we found that solanine inhibited cancer cells growth through caspase-3 dependent mitochondrial apoptosis. Mechanically, solanine promotes the opening of mitochondrial membrane permeability transition pore (MPTP) by downregulating the Bcl-2/Bax ratio; thereafter, Cytochrome c and Smac are released from mitochondria into cytosol to process the caspase-3 zymogen into an activated form. Moreover, we found that the expression of tumor metastasis related proteins, MMP-2 and MMP-9, was also decreased in the cells treated with solanine. Therefore, our results suggested that solanine was an effective compound for the treatment of pancreatic cancer.
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Regional arterial infusion with lipoxin A4 attenuates experimental severe acute pancreatitis.
PLoS ONE
PUBLISHED: 01-01-2014
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Investigate the therapeutic effect of regional arterial infusion (RAI) with Aspirin-Triggered Lipoxin A4 (ATL) in experimental severe acute pancreatitis (SAP) in rats.
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Antitumor efficacy of ?-solanine against pancreatic cancer in vitro and in vivo.
PLoS ONE
PUBLISHED: 01-01-2014
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?-solanine, a steroidal glycoalkaloid in potato, was found to have proliferation-inhibiting and apoptosis-promoting effect on multiple cancer cells, such as clone, liver, melanoma cancer cells. However, the antitumor efficacy of ?-solanine on pancreatic cancer has not been fully evaluated. In this study, we inquired into the anti-carcinogenic effect of ?-solanine against human pancreatic cancer cells. In the present study, we investigated the anti-carcinogenic effect of ?-solanine against human pancreatic cancer cells. In vitro, ?-solanine inhibited proliferation of PANC-1, sw1990, MIA PaCa-2 cells in a dose-dependent manner, as well as cell migration and invasion with atoxic doses. The expression of MMP-2/9, extracellular inducer of matrix metalloproteinase (EMMPRIN), CD44, eNOS and E-cadherin were suppressed by ?-solanine in PANC-1 cells. Moreover, significantly decreased vascular endothelial growth factor (VEGF) expression and tube formation of endothelial cells were discerned following ?-solanine treatment. Suppressed phosphorylation of Akt, mTOR, and Stat3, and strengthen phosphorylation of ?-catenin was found, along with markedly decreased tran-nuclear of NF-?B, ?-catenin and TCF-1. Following the administration of ?-solanine (6 µg/g for 2 weeks) in xenograft model, tumor volume and weight were decreased by 61% and 43% (p<0.05) respectively, showing decreased MMP-2/9, PCNA and VEGF expression. In conclusion, ?-solanine showed beneficial effects on pancreatic cancer in vitro and in vivo, which may via suppressing the pathway proliferation, angiogenesis and metastasis.
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Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury.
Exp. Biol. Med. (Maywood)
PUBLISHED: 09-02-2013
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Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor ? (TNF-?) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-?-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-?B/p65 (NF-?B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-? stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-?-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-?B and p38 MAPK and up-regulation of cytoprotective HO-1.
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The efficiency of continuous regional intra-arterial infusion in the treatment of infected pancreatic necrosis.
Pancreatology
PUBLISHED: 02-15-2013
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Our aim was to investigate the efficiency of continuous regional intra-arterial infusion (CRAI) with antisecretory agents and antibiotics in the treatment of infected pancreatic necrosis.
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Single-layer anastomosis without hemostasis in the submucosa layer by electric coagulation or ligation: a novel technique of anastomosis for all gastrointestinal tracts.
Hepatogastroenterology
PUBLISHED: 04-23-2011
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Single-layer anastomosis has been used extensively for all gastrointestinal tracts around the world. Until now, most surgeons take for granted that submucous layers need careful hemostasis either by electric coagulation or ligation for the prevention of anastomotic stoma bleeding. We experienced hemostasis in the submucosa layer by adequate strength of anastomosis rather than electric coagulation for gastrointestinal tracts. In the present study the safety and benefit of this novel anastomotic technique was evaluated. From 1994 to 2006, 527 gastrointestinal anastomosis were performed using the improved anastomotic technique, and 281 anastomosis (control group) were completed with the commonly adopted technique. The improved anastomotic technique could decreased the incidence of leaks (p = 0.024), and the procedure time required for anastomosis in comparison to control group (p = 0.0002). The incidence of abscesses (p = 0.51) and bleeding (p = 1.00) of the improved anastomotic technique were no significantly different between the groups. The novel technique, single-layer anastomosis without hemostasis in the submucosa layer by electric coagulation or ligation, is suitable for all gastrointestinal anastomosises and it should be popularized.
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The protective effects of Lipoxin A4 during the early phase of severe acute pancreatitis in rats.
Scand. J. Gastroenterol.
PUBLISHED: 10-18-2010
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Our aim was to investigate the protective effects of a Lipoxin A(4) analogue (LXA4) in the early phase of acute pancreatitis in rats.
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Single-layer anastomosis without hemostasis in the submucosa layer by electric coagulation or ligation: a novel technique of anastomosis for all gastrointestinal tracts.
Hepatogastroenterology
PUBLISHED: 10-12-2010
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Single-layer anastomosis has been used extensively for all gastrointestinal tract around the world. Up to now, most of surgeons take it for granted that submucous layers need careful hemostasis either by electric coagulation or ligation for prevention of anastomotic stoma bleeding. We experienced hemostasis in the submucosa layer by adequate strength of anastomosis rather than electric coagulation for gastrointestinal tracts. In the present study was evaluated the safety and benefit of this novel anastomotic technique.
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The conformation change of Bcl-2 is involved in arsenic trioxide-induced apoptosis and inhibition of proliferation in SGC7901 human gastric cancer cells.
World J Surg Oncol
PUBLISHED: 04-20-2010
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Arsenic trioxide has been established as a first-line agent for treating acute promyelocytic leukemia. Experimental data suggest that arsenic trioxide also can have a potential use as chemotherapeutic agent for other malignancies. The precise mechanisms of action of arsenic trioxide have though not been elucidated. As the role of Bcl-2 in arsenic trioxide-mediated cell apoptosis and conformation change of Bcl-2 in response to arsenic trioxide treatment has not been studied. The aim of the present study was to determine whether conformation change of Bcl-2 is involved in the action of arsenic trioxide.
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Total gastrointestinal tract necrosis after ingesting a considerable amount of hydrochloric acid.
J. Gastrointest. Surg.
PUBLISHED: 06-26-2009
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It has not been reported that ingesting large amounts of strong acid resulted in total gastrointestinal tract necrosis. Here we describe a case of a man with total gastrointestinal tract necrosis after ingestion of a considerable amount of hydrochloric acid.
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A modified canine model of portal hypertension with hypersplenism.
Scand. J. Gastroenterol.
PUBLISHED: 06-17-2009
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The aim of this study was to develop and describe an experimental canine model of portal hypertension with hypersplenism.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.