In ex vivo and in vivo models, decreased osmolarity and charge density increased RF energy delivery to tissue, resulting in larger lesions for both open and closed irrigated ablations. A perpendicular catheter position created larger lesions across all irrigants for both open and closed irrigation ablation. The incidence of steam pops was observed more frequently with high power open irrigated using D5W, especially if the catheter was in a perpendicular position. Further research is required to evaluate any clinical role for using different irrigants with an externally irrigated catheter.
Myocardial tissue treated with CNTs resulted in significantly larger lesions at both low and high power settings. The electrical and thermal conductivity of heat generated by application of RF in myocardial tissue was altered by the presence of CNTs. Further research is needed to assess the in vivo applicability for this concept of facilitated ablation with CNTs.
Aim: Fluopsin C, an antibiotic isolated from Pseudomonas jinanesis, has shown antitumor effects on several cancer cell lines. In the current study, the oncotic cell death induced by fluopsin C was investigated in human breast adenocarcinoma cells in vitro. Methods: Human breast adenocarcinoma cell lines MCF-7 and MD-MBA-231 were used. The cytotoxicity was evaluated using MTT assay. Time-lapse microscopy and transmission electron microscopy were used to observe the morphological changes. Cell membrane integrity was assessed with propidium iodide (PI) uptake and lactate dehydrogenase (LDH) assay. Flow cytometry was used to measure reactive oxygen species (ROS) level and mitochondrial membrane potential (Δψm). A multimode microplate reader was used to analyze the intracellular ATP level. The changes in cytoskeletal system were investigated with Western blotting and immunostaining.Results: Fluopsin C (0.5-8 μmol/L) reduced the cell viability in dose-and time-dependent manners. Its IC 50 values in MCF-7 and MD-MBA-231 cells at 24 h were 0.9 and 1.03 μmol/L, respectively. Fluopsin C (2 μmol/L) induced oncosis in both the breast adenocarcinoma cells characterized by membrane blebbing and swelling, which was blocked by pretreatment with the pan-caspase inhibitor Z-VAD-fmk. In MCF-7 cells, fluopsin C caused PI uptake into the cells, significantly increased LDH release, induced cytoskeletal system degradation and ROS accumulation, decreased the intracellular ATP level and Δψm. Noticeably, fluopsin C exerted comparable cytotoxicity against the normal human hepatocytes (HL7702) and human mammary epithelial cells with the IC 50 values at 24 h of 2.7 and 2.4 μmol/L, respectively. Conclusion: Oncotic cell death was involved in the anticancer effects of fluopsin C on human breast adenocarcinoma cells in vitro. The hepatoxicity of fluopsin C should not be ignored.
Telekin, a eudesmane-type sesquiterpene lactone compound isolated from Chinese folk medicine Carpesium divaricatum, has been reported to strongly inhibit the proliferation of cancer cells. In this study, the involvement of a mitochondria-mediated pathway in the pro-apoptotic action of telekin was investigated in human hepatocellular carcinoma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays showed that telekin exhibited excellent anti-proliferation activity in hepatocellular carcinoma cells and low cytotoxicity to normal hepatocyte cells. Telekin-induced apoptosis was characterized by chromatin condensation, formation of apoptotic bodies, and exposure of phosphatidylserine on the extracellular surface, as revealed by 4,6-diamidino-2-phenylindole (DAPI) nuclear staining and flow cytometry. Flow cytometry analysis showed that telekin induced the loss of mitochondrial membrane potential (MMP), as well as increased the levels of intracellular free calcium and reactive oxygen species (ROS). Additionally, Western blot results demonstrated that telekin induced the decrease in Apaf-1 and Bcl-2 expression, increase in Bax expression, release of cytochrome C, and activation of caspase-9 and caspase-3 in HepG-2 cells. These findings indicate that telekin activates the mitochondria-mediated apoptotic pathway in hepatocellular carcinoma cells and may merit further investigation as a potential therapeutic agent for the treatment of hepatocellular carcinoma.Key words telekin; Carpesium divaricatum; apoptosis; hepatocellular carcinoma; mitochondria Hepatocellular carcinoma (HCC) is one of the most frequent primary tumors in adults with a high mortality rate worldwide.1,2) Chemotherapy is currently the most common and effective strategy against HCC in the clinical field. A number of anticancer drugs derived from natural products, such as taxane, vinca alkaloid, and hydroxyl-camptothecin, have exhibited excellent anticancer potential.3) Telekin is isolated from Carpesium divaricatum, which has long been used as Chinese folk medicine given its antipyretic, analgesic, vermifugic, and anti-inflammatory properties.4) In China, the whole C. divaricatum plant is used in medicine as febrifuge and astringent. It is also used to treat colds, wind syndrome of the head, sore throat, toothache, mumps, hemorrhoids, and malaria.5) Telekin has also been reported to exhibit strong antitumor activity in several human carcinoma cell lines. 6,7)Apoptosis is a genetically controlled and evolutionarily conserved process of cell death. Cells undergoing apoptosis are characterized by membrane blebbing, cytoplasmic shrinkage, DNA fragmentation, and apoptotic body formation. [8][9][10] This process is also most frequently taken as a major pathway for chemotherapeutics to combat cancer cells. Therefore, searching for agents that can trigger tumor cells apoptosis has become an attractive strategy in anti-cancer drug discovery.Molecular biological studies indicate that extrinsically and intrinsically mediated pathways cause a...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.