cytellin has been researched along with Liver-Neoplasms* in 13 studies
13 other study(ies) available for cytellin and Liver-Neoplasms
Article | Year |
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Evaluation of Anti-Hepatocellular-Cancer Properties of β-Sitosterol and β-Sitosterol-Glucoside from Indigofera zollingeriana Miq.
Liver cancer is the most frequent cancer, making it the leading cause of cancer death globally. Traditional medicinal plants with anticancer properties can be used as drugs or dietary adjuvants to existing therapies. This chapter presents a protocol for the preparation of β-sitosterol and β-sitosterol-glucoside from Indigofera zollingeriana Miq (I. zollingeriana) and the evaluation of these for anticancer activity in hepatocellular cells. Topics: Carcinoma, Hepatocellular; Glucosides; Humans; Indigofera; Liver Neoplasms; Plant Extracts; Sitosterols | 2022 |
Assessments of
β-sitosterol (BS), a phytosterol, exhibits ameliorative effects on hepatocellular carcinoma (HCC) due to its antioxidant activities. However, its poor aqueous solubility and negotiated bioavailability and short elimination half-life is a huge limitation for its therapeutic applications. To overcome these two shortcomings, BS-loaded niosomes were made to Topics: Animals; Antineoplastic Agents; Carcinoma, Hepatocellular; Drug Carriers; Liposomes; Liver Neoplasms; Polyethylene Glycols; Rats; Sitosterols | 2021 |
Strobilanthes crispus bioactive subfraction inhibits tumor progression and improves hematological and morphological parameters in mouse mammary carcinoma model.
Locally known as 'pecah batu', 'bayam karang', 'keci beling' or 'batu jin', the Malaysian medicinal herb, Strobilanthes crispus (S. crispus), is traditionally used by the local communities as alternative or adjuvant remedy for cancer and other ailments and to boost the immune system. S. crispus has demonstrated multiple anticancer therapeutic potential in vitro and in vivo. A pharmacologically active fraction of S. crispus has been identified and termed as F3. Major constituents profiled in F3 include lutein and β-sitosterol.. In this study, the effects of F3, lutein and β-sitosterol on tumor development and metastasis were investigated in 4T1-induced mouse mammary carcinoma model.. Tumor-bearing mice were fed with F3 (100 mg/kg/day), lutein (50 mg/kg/day) and β-sitosterol (50 mg/kg/day) for 30 days (n = 5 each group). Tumor physical growth parameters, animal body weight and development of secondary tumors were investigated. The safety profile of F3 was assessed using hematological and histomorphological changes on the major organs in normal control mice (NM).. Our findings revealed significant reduction of physical tumor growth parameters in all tumor-bearing mice treated with F3 (TM-F3), lutein (TM-L) or β-sitosterol (TM-β) as compared with the untreated group (TM). Statistically significant reduction in body weight was observed in TM compared to the NM or treated (TM-F3, TM-L and TM-β) groups. Histomorphological examination of tissue sections from the F3-treated group showed normal features of the vital organs (i.e., liver, kidneys, lungs and spleen) which were similar to those of NM. Administration of F3 to NM mice (NM-F3) did not cause significant changes in full blood count values.. F3 significantly reduced the total tumor burden and prevented secondary tumor development in metastatic breast cancer without significant toxicities in 4T1-induced mouse mammary carcinoma model. The current study provides further support for therapeutic development of F3 with further pharmacokinetics studies. Topics: Acanthaceae; Animals; Antineoplastic Agents, Phytogenic; Breast Neoplasms; Cell Line, Tumor; Female; Kidney Neoplasms; Liver Neoplasms; Lung Neoplasms; Lutein; Mice, Inbred BALB C; Plant Extracts; Sitosterols; Splenic Neoplasms; Tumor Burden | 2021 |
β-Sitosterol-assisted silver nanoparticles activates Nrf2 and triggers mitochondrial apoptosis via oxidative stress in human hepatocellular cancer cell line.
Cancer nanomedicine is an emerging field of cancer therapeutics. Incidence of hepatocellular carcinoma (HCC) is increasing worldwide, and currently, it is the second leading cause of cancer-related deaths. This study investigates the cytotoxic potential of β-sitosterol-assisted silver nanoparticles (BSS-SNPs) in HepG2 cells. The silver nanoparticles were synthesized using β-sitosterol as a reducing and stabilizing agent. The characterization of BSS-SNPs was done by UV-visible spectrophotometry and transmission electron microscope (TEM) analysis. HepG2 cells were treated with different concentrations of BSS-SNPs for 24 hr, and cytotoxicity was evaluated by MTT assay. Intracellular ROS was investigated by 2',7'-dichlorofluorescin diacetate staining. The nuclear factor erythroid 2-related factor 2 (Nrf-2) protein expression was investigated by immunofluorescence staining. Morphology-related to apoptotic changes were analyzed by annexin V staining. Intrinsic apoptosis pathwayrelated molecular markers were investigated by western blotting and PCR analysis. Spectrophotometry analysis confirmed a strong absorption peak at 420 nm, which showed the successful synthesis of BSS-SNPs. The TEM analysis indicated the spherical-, rod-, and hexagonal BSS-SNPs with the size ranges from 5 to 55 nm. BSS-SNPs significantly inhibited the proliferation and induced ROS and Nrf-2 expression in HepG2 cells. BSS-SNPs treatment caused apoptosis-related morphological changes and upregulated the pro-apoptotic markers such as bax, p53, cytochrome c, and caspases-9, -3 and downregulated bcl-2 expressions. Our findings suggest that BSS-SNPs might serve as potential drug candidates for HCC. Topics: Antineoplastic Agents; Apoptosis; Carcinoma, Hepatocellular; Hep G2 Cells; Humans; Liver Neoplasms; Mitochondria; Nanoparticles; NF-E2-Related Factor 2; Oxidative Stress; Silver; Sitosterols | 2020 |
Phytosterol, Lipid and Phenolic Composition, and Biological Activities of Guava Seed Oil.
Plant seeds have been found to contain bioactive compounds that have potential nutraceutical benefits. Guava seeds ( Topics: Animals; Antioxidants; Carcinoma, Hepatocellular; Cholesterol; Female; Hexanes; Liver Neoplasms; Male; Oxidative Stress; Phenols; Phytosterols; Plant Extracts; Plant Oils; Psidium; Rats; Seeds; Sitosterols; Triglycerides | 2020 |
Regulatory Mechanisms of Coicis Semen on Bionetwork of Liver Cancer Based on Network Pharmacology.
At present, there is an increasing incidence and mortality of liver cancer. Despite surgery and chemoradiotherapy, there is a lack of effective oral medications with low side effects. In East Asia, Coicis Semen (CS) is used as both food and natural medicine and has a significant impact on the treatment of liver cancer. However, due to its multicomponent and multitarget characteristics, the mechanisms of CS against liver cancer remain unclear. This study collected CS compounds and target proteins in SymMap, then cross-matched with the liver cancer targets in the CTD database to construct an interaction network of CS-liver cancer proteins, and visualized by Cytoscape software. DAVID database was used to perform pathway enrichment analysis to find target proteins in core pathways and the related small molecules in CS. The results showed that a total of 103 common genes shared by CS and liver cancer were obtained, which were enriched for precancerous lesion pathways such as hepatitis B and fatty liver and biological signaling pathways such as HIF-1 and TNF. The combination of sitosterol and CASP3 in CS, acting on "pathways in cancer" and restoring normal cell apoptosis, could be the core mechanisms of CS in the treatment of liver cancer. Based on the system biology analysis, it is speculated that CS may not only participate in multiple mechanisms of action to treat liver cancer synergistically but may also be involved in factors that reduce the incidence of liver cancer. Topics: Carcinoma, Hepatocellular; Caspase 3; Coix; Gene Ontology; Humans; Liver Neoplasms; Sitosterols; Small Molecule Libraries; Sorafenib | 2020 |
Daucosterol Inhibits the Proliferation, Migration, and Invasion of Hepatocellular Carcinoma Cells via Wnt/β-Catenin Signaling.
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. The purpose of this study was to determine the effects of daucosterol on HCC by investigating Wnt/β-catenin signaling. In this study, HepG2 and SMMC-7721 cells were treated with varying concentrations of daucosterol, and the corresponding inhibitory effects on HCC cells were examined via CCK-8 assays. Cell migration and invasion abilities were detected via transwell assays. β-Catenin and phospho (p)-β-catenin levels were analyzed via western blotting. Our results showed that daucosterol reduced the proliferation, migration, and invasion capacities of HCC cells in a concentration-dependent manner. In addition, daucosterol reduced the levels of β-catenin and p-β-catenin in HepG2 and SMMC-7721 cells. Furthermore, the Wnt signaling pathway inhibitor SB-216763 was used to treat HepG2 and SMMC-7721 cells with daucosterol. Our results showed that co-treatment with daucosterol and SB-216763 abolished the effects of daucosterol on cell inhibition ratios, cell migration, and cell invasion. These findings indicated that daucosterol inhibited cell migration and invasion in HCC cells via the Wnt/β-catenin signaling pathway. Therefore, our study highlights the use of daucosterol as a promising therapeutic strategy for HCC treatment. Topics: beta Catenin; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; Liver Neoplasms; Sitosterols; Wnt Proteins; Wnt Signaling Pathway | 2017 |
Comparing different sterol containing solid lipid nanoparticles for targeted delivery of quercetin in hepatocellular carcinoma.
Quercetin (QT) is a potential chemotherapeutic drug with low solubility that seriously limits its clinical use. The aim of this study was enhancing cellular penetration of QT by sterol containing solid lipid nanoparticles (SLNs) which make bilayers fluent for targeting hepatocellular carcinoma cells. Three variables including sterol type (cholesterol, stigmasterol and stigmastanol), drug and sterol content were studied in a surface response D-optimal design for preparation of QT-SLNs by emulsification solvent evaporation method. The studied responses included particle size, zeta potential, drug loading capacity and 24 h release efficiency (RE24%). Scanning electron and atomic force microscopy were used to study the morphology of QT-SLNs and their thermal behavior was studied by DSC analysis. Cytotoxicity of QT-SLNs was determined by MTT assay on HepG-2 cells and cellular uptake by fluorescence microscopy method. Optimized QT-SLNs obtained from cholesterol and QT with the ratio of 2:1 that showed particle size of 78.0 ± 7.0 nm, zeta potential of -22.7 ± 1.3 mV, drug loading efficiency of 99.9 ± 0.5% and RE24 of 56.3 ± 3.4%. IC50 of QT in cholesterol SLNs was about six and two times less than free QT and phytosterol SLNs, respectively, and caused more accumulation of QT in HepG2 cells. Blank phytosterol SLNs were toxic on cells. Topics: Antineoplastic Agents, Phytogenic; Carcinoma, Hepatocellular; Chemistry, Pharmaceutical; Cholesterol; Hep G2 Cells; Humans; Liposomes; Liver Neoplasms; Nanoparticles; Particle Size; Quercetin; Sitosterols; Stigmasterol | 2014 |
[Antiproliferative effects mechanism of beta-sitosterul in hepatoma HepG2 cells].
To study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells.. Cell proliferation was assessed by MTT assay. Cell cycle distribution, apoptosis and mitochondrial membrane potential were measured by high content screening (HCS). The protein expression of caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome c in the HepG2 cells were evaluated by Western Blots.. beta-Sitosterul exerted significant antiproliferative effects in HepG2 cells. Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein. However, beta-sitosterul had hardly any effects on QSG7701 cells.. beta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway. Topics: Antineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Carcinoma, Hepatocellular; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Hep G2 Cells; Humans; Liver Neoplasms; Membrane Potential, Mitochondrial; Sitosterols | 2011 |
Cytotoxic and apoptotic effects of single and mixed oxides of beta-sitosterol on HepG2-cells.
While health implications caused by cholesterol oxidation products (COPs) seem to be generally accepted, research on phytosterol oxidation products (POPs) is still limited. Since POPs are commercially not available knowledge on their toxic activities is mainly derived from blends instead of pure compounds. Therefore the aim of the present study was to examine the cytotoxicity of three individual oxidation products of beta-sitosterol, 7-ketositosterol, 7beta-OH-sitosterol, 7alpha-OH-sitosterol, a mixture of 6beta-OH-3-keto-sitosterol/6alpha-OH-3-keto-sitosterol (ratio 4:3) and a mixture of polar oxides towards HepG2-cells. All tested compounds were found to reduce cell viability in a significant and concentration dependent way, particularly 7-keto- and 7alpha-OH-sitosterol showed to be highly active. Only for 7-ketositosterol an increase in early apoptotic cells was observed. Enhancement of O(2)(-) production was assessed for all oxides, whereas malondialdehyd (MDA) levels were increased by 7-keto- and 7alpha-OH-sitosterol only. However, cell death did not appear to be necessarily dependent on the generation of oxidative stress. Further no DNA strand breaks were observed with the COMET assay. By assessing the accumulation of single oxidation products in the cells a link between higher proportions of oxides inside the cells and their cytotoxic potential could be found. Topics: Apoptosis; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Survival; Comet Assay; DNA Breaks; Dose-Response Relationship, Drug; Humans; Liver Neoplasms; Oxidation-Reduction; Oxidative Stress; Oxides; Sitosterols | 2009 |
Suppression of hepatitis B virus-derived human hepatocellular carcinoma by NF-kappaB-inducing kinase-specific siRNA using liver-targeting liposomes.
Hepatitis B virus triggers an increase of NF-kappaB inducing kinase (NIK)-dependent NF-kappaB activation, followed by the promotion of hepatocellular carcinoma (HCC). Here, we examined the inhibitory effect of NIK-specific siRNA on NF-kappaB signaling and HCC. The results of this study indicated that these siRNAs suppressed HBV-derived HCC by regulating NIK activation. To exert a protective effect from degradation enzyme, cationic liposomes were contrived and modified to contain beta-sitosterol glucoside to target the asialoglycoprotein receptors in liver cancer cells. The cationic dimyristoyl diacyltrimethylammonium propane liposomes were prepared by a reverse-phase evaporation method with slight modification. beta-Sitosterol glucoside was added to the lipid mixture at the beginning of the liposome preparation for the purpose of liver targeting. These liposomes assisted the delivery of the siRNA to specific cells and protected it from various lyases, followed by the ultimate suppression of HCC. Topics: Asialoglycoprotein Receptor; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Proliferation; Cell Survival; Genetic Therapy; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Lipids; Liposomes; Liver Neoplasms; Lyases; NF-kappaB-Inducing Kinase; Protein Serine-Threonine Kinases; RNA Interference; RNA, Messenger; RNA, Small Interfering; Sitosterols; Time Factors; Transfection | 2009 |
Margarine phytosterols decrease the secretion of atherogenic lipoproteins from HepG2 liver and Caco2 intestinal cells.
Several studies in humans have demonstrated the hypocholesterolemic effect of plant sterol consumption. It is unclear whether plant sterols regulate lipoprotein metabolism in the liver and intestines, thereby decreasing the levels of circulating atherogenic lipoproteins. We investigated the effect of the three main phytosterols: stigmasterol, campesterol, and beta-sitosterol on lipoprotein production in HepG2 human liver cells and Caco2 human intestinal cells and the mechanisms involved. Cells were incubated for 24h with 50 micromol/L of the different phytosterols or 10 micromol/L of atorvastatin. Very low-density lipoprotein levels (measured by apolipoprotein (apo) B100) in HepG2 cells and chylomicron levels (measured by apoB48) in Caco2 cells were measured using western blotting. Intracellular cholesterol levels were measured using gas chromatography. Analysis was carried out using Student's t-test and ANOVA. Secretion levels of apoB100 significantly decreased by approximately 30% after incubation with all phytosterols compared to control. In addition, cholesterol ester (CE) concentrations significantly decreased when HepG2 cells were incubated with the phytosterols compared to control cells. Secretion of apoB48 from intestinal cells significantly decreased by 15% with stigmasterol, 16% with campesterol and 19% beta-sitosterol compared to control. Collectively the data suggests that plant sterols limit lipid (CE) availability in cells. Decreases in circulating levels of LDL and chylomicron remnants seen in humans with the consumption of margarine phytosterols are possibly due to their effect on lipid production in cells and would therefore reduce the risk of developing cardiovascular disease. Topics: Anticholesteremic Agents; Apolipoprotein B-100; Apolipoprotein B-48; Apolipoproteins B; Atherosclerosis; Atorvastatin; Caco-2 Cells; Carcinoma, Hepatocellular; Cholesterol; Drug Synergism; Enterocytes; Hepatocytes; Heptanoic Acids; Humans; Liver Neoplasms; Margarine; Phytosterols; Pyrroles; Sitosterols; Stigmasterol | 2005 |
Liver targeting liposomes containing beta-sitosterol glucoside with regard to penetration-enhancing effect on HepG2 cells.
The aim of this study was to examine the interaction of soybean-derived sterylglucoside (SG) with the human hepatoblastoma cell line HepG2 with regard to the penetration-enhancing effect of beta-sitosterol glucoside (Sit-G) to clarify the accumulation of SG-containing liposomes (SG-liposomes) to the liver in vivo. The approach was based on measurement of the association of SG-liposomes labeled with 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (Dil) in terms of asialoglycoprotein receptor (ASGP-R)-mediated endocytosis, affinity of Sit-G using lAsys and the association of FITC-dextran 4400 (FD-4) increased by Sit-G with the cells. The association of SG-liposomes was decreased by addition of asialofetuin, suggesting that SG-liposomes might be taken up via ASGP-R. Sit-G showed higher affinity with HepG2 cells than HeLa cells, and enhanced the association of FD-4 depending on the incubation time and Sit-G concentrations. Significant positive correlations were found between Sit-G and FD-4 association with the cells, indicating that Sit-G enhanced the drug penetration by distribution in cell membranes. The high degree of liver association of SG-liposomes in vivo might be related to recognition of glucose residues of SG by ASGP-R and to the high affinity and penetration-enhancing effect of Sit-G with hepatocytes. Topics: alpha-Fetoproteins; Asialoglycoprotein Receptor; Asialoglycoproteins; Binding, Competitive; Carcinoma, Hepatocellular; Cell Membrane; Cell Membrane Permeability; Excipients; Fetuins; Fluorescein-5-isothiocyanate; Humans; Liposomes; Liver; Liver Neoplasms; Sitosterols; Tumor Cells, Cultured | 2002 |