In Vitro and In Vivo Antitumor Activity of Silver Nanoparticles on B16 Melanoma

NANO ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. 2050163
Author(s):  
Hongkun Gao ◽  
Ping Fan ◽  
Qizhen Xu ◽  
Yiting Li ◽  
Jianxin Wang ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Antitumor Activity ◽  
Antimicrobial Agents ◽  
Malignant Tumors ◽  
Annexin V ◽  
In Vitro Study ◽  
B16 Melanoma ◽  
Potential Strategy

Melanoma, one of the most malignant tumors, is difficult to treat due to its high drug resistance. Silver nanoparticles (AgNPs) are widely used as antimicrobial agents in biomedical fields. In this study, the spherical AgNPs with average sizes of 5[Formula: see text]nm were prepared using a dopamine reduction method. The in vitro study shows that AgNPs with the concentrations of 0.5[Formula: see text][Formula: see text]g/mL and 1[Formula: see text][Formula: see text]g/mL exhibit good biocompatibility to 3T3L1 fibroblast cells. AgNPs with the same concentrations significantly inhibited the growth of B16 melanoma cells. In culture with B16 cells, AgNPs induced intracellular oxidative stress by generating the reactive oxygen species and reducing the superoxide dismutase, which further reduces the mitochondrial membrane potential. Moreover, the damage in mitochondria could activate mitochondrion-mediated cell apoptosis. The B16 cells apoptosis was analyzed by FITC-Annexin V/propidium iodide double staining assay, which confirms that AgNPs caused the abundance of apoptotic cells in different stages. Thus, AgNPs displayed the antitumor activity in vitro. Then, the therapeutic efficacy in vivo was evaluated in mice-bearing B16 melanoma tumors. The obtained results show the antitumor ability of AgNPs and provide a potential strategy for cancer treatment.

scholarly journals Shengma Biejia Decoction Inhibits Cell Growth in Multiple Myeloma by Inducing Autophagy-Mediated Apoptosis Through the ERK/mTOR Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Huibo Dai ◽  
Bangyun Ma ◽  
Xingbin Dai ◽  
Jie Pang ◽  
Jingyu Wang ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Caspase 3 ◽  
Malignant Tumors ◽  
Xenograft Model ◽  
Annexin V ◽  
Mtor Pathway ◽  
Therapy Strategy ◽  
Related Proteins

Shengma Biejia decoction (SMBJD), a traditional Chinese formula recorded in the Golden Chamber, has been widely used for the treatment of malignant tumors. However, its underlying molecular targets and mechanisms are still unclear. This study showed that SMBJD inhibited tumor growth and stimulated hemogram recovery significantly in a multiple myeloma xenograft model. Western blot and immunohistochemistry assays of tumor tissues showed that SMBJD reduced the ratio of autophagy-related proteins LC3-II/LC3-I, while P62 and apoptosis-related proteins cleaved caspase-3/caspase-3 and Bax/Bcl-2 were upregulated. In vitro experiments demonstrated the time-dependent and dose-dependent cytotoxicity of SMBJD on multiple myeloma cell lines H929 and U266 through MTT assays. The LC3-II/LC3-I ratio and number of GFP-LC3 puncta showed that SMBJD inhibited the autophagy process of H929 and U266 cells. Moreover, both SMBJD and 3-methyladenine (3-MA) caused a decrease in LC3-II/LC3-I, and SMBJD could not reverse the upregulation of LC3-II/LC3-I caused by bafilomycin A1 (Baf-A1). Furthermore, the results of annexin V-FITC and propidium iodide double staining demonstrated that SMBJD treatment induced the apoptosis of H929 and U266 cells. These data prove that SMBJD inhibits autophagy and promotes apoptosis in H929 and U266 cells. The results also show that rapamycin could reduce the rate of SMBJD-induced apoptosis in H929 and U266 cells, at a concentration which had no effect on apoptosis but activated autophagy. In addition, analysis of the mechanism indicated that levels of phosphorylated ERK and phosphorylated mTOR were increased by treatment with SMBJD in vivo and in vitro. These results indicate that SMBJD, an old and effective herbal compound, could inhibit the viability of H929 and U266 cells and induce autophagy-mediated apoptosis through the ERK/mTOR pathway. Thus, it represents a potential therapy strategy for multiple myeloma.

In vitro and in vivo Enhancement of Vincristine Antitumor Activity on B16 Melanoma Cells by Calcium Antagonist Flunarizine

Oncology ◽  
1987 ◽  
Vol 44 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Alberto Bellelli ◽  
Claudia Camboni ◽  
Giovanna de Luca ◽  
Mario Materazzi ◽  
Manlio Mattioni ◽  
...  
Keyword(s):  
Calcium Antagonist ◽  
Antitumor Activity ◽  
Melanoma Cells ◽  
B16 Melanoma ◽  
B16 Melanoma Cells

scholarly journals Antimicrobial applications of nanoliposome encapsulated silver nanoparticles: a potential strategy to overcome bacterial resistance

2020 ◽  
Vol 16 ◽  
Author(s):  
M.R. Mozafari ◽  
Sarabanou Torkaman ◽  
Fatemeh Mahsa Karamouzian ◽  
Babak Rasti ◽  
Bikash Baral
Keyword(s):  
Silver Nanoparticles ◽  
Bacterial Infections ◽  
Bacterial Resistance ◽  
Water Soluble ◽  
Severe Illness ◽  
Efficient System ◽  
Antimicrobial Substances ◽  
Potential Strategy

: Bacterial infections result in hundreds of million cases of severe illness annually worldwide. Rapidly increasing drug resistance of pathogens further aggravates this threat to human health and warrants the search for effective broadspectrum antibacterial agents. Silver metal has a long history of application in human medicine and healthcare. In ancient times, silver was employed as a disinfectant for water purification and storage while it is still being used as an antimicrobial ingredient in some nanotechnology-based products. Encapsulation of antimicrobial substances such as silver nanoparticles in nanoliposomes could provide protection and targeting for the encapsulated or entrapped material. Nanoliposomes are biocompatible and biodegradable drug delivery systems with the ability to encapsulate both lipidsoluble and water-soluble compounds, as well as metal ions. Furthermore, nanoliposomes have been shown to be able to deliver encapsulated agents to target bacteria in vitro as well as in vivo. In this review, we present the use of nanoliposome-encapsulated silver nanoparticles as an efficient system for antibacterial applications.

Cyanidin 3-O-Glucoside Induces the Apoptosis in the Osteosarcoma Cells through Upregulation of the PPARγ and P21: An In Vitro Study

2020 ◽  
Vol 20 (9) ◽  
pp. 1087-1093
Author(s):  
Hesam A. Atashi ◽  
Hamid Z. Arani ◽  
Amirhossein Shekarriz ◽  
Hamidreza Nazari ◽  
Amirhossein Zabolian ◽  
...  
Keyword(s):  
Real Time ◽  
Cell Lines ◽  
Mtt Assay ◽  
Malignant Tumors ◽  
Apoptotic Cell ◽  
Annexin V ◽  
In Vitro Study ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells

Background: Osteosarcoma (OS) is known as the malignant tumors in the bone. Cyanidin 3-OGlucoside (C3G) has a potential to induce the apoptotic cell death in different cancer cells; however, the mechanisms of action for C3G have not been clarified yet. Objective: In this study, the apoptotic effects of C3G on three different osteosarcoma cell lines including Saso-2, MG-63, and G-292 (clone A141B1) were investigated. Methods: The 24-hr IC50 of C3G for Saso-2, G-292, and MG-63 cells was evaluated by the MTT assay. Apoptosis induction in these cell lines after treatment with the C3G was approved by the Annexin V/PI flow cytometry. Changes at the mRNA expression level of PPARγ, P21, Bax, and Bcl-xl genes were investigated by real-time Polymerase Chain Reaction (PCR) technique, and P21 expression was further confirmed by the western blotting. Results: The MTT assay results demonstrated that the 24-hr IC50 of C3G was equal to 110μg/ml for Saso-2 and G-292 cells while it was about 140μg/ml for the MG-63 cells. The results of real-time PCR clearly showed that treatment of the cells with 24hrs IC50 of C3G caused the upregulation of PPARγ, P21, and Bax genes. Moreover, western blot analysis confirmed that P21 protein overexpressed endogenously after treatment of the cells with the C3G, and it was more upregulated in the MG-63 cells compared to the other cell lines. Conclusion: According to the findings of the study, the C3G is a novel anti-osteosarcoma agent with the ability to induce the apoptosis in different osteosarcoma cells through upregulation of the PPARγ and P21 genes.

Evaluation of Antitumor Activity and Hepatoprotective Effect of Mitomycin C Solubilized in Chamomile Oil Nanoemulsion

2019 ◽  
Vol 19 (10) ◽  
pp. 1232-1242
Author(s):  
Waad A. Al-Otaibi ◽  
Mayson H. Alkhatib ◽  
Abdulwahab N. Wali
Keyword(s):  
Antitumor Activity ◽  
In Vitro Study ◽  
Ehrlich Ascites Carcinoma ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Hepatoprotective Effect ◽  
Antineoplastic Effect

:The present study aimed to investigate the antitumor activity and hepatoprotective effect of the MTC, when combined with CHAM oil nanoemulsion (NE), (CHAM-MTC) on the tumor growth.Materials/Methods:The in vitro study assessed the antineoplastic effect of CHAM-MTC on the MCF-7 breast cancer cells while the in vivo therapeutic effectiveness and toxicities of CHAM-MTC were evaluated in Ehrlich Ascites Carcinoma (EAC) bearing mice. One hundred female Swiss albino mice, divided equally into non-EAC group (negative control), untreated EAC group (positive control) and three EAC groups received once intraperitoneal injection of 0.2ml CHAM-NE, 0.2ml Normal Saline (NS) contained MTC (1mg/kg) and 0.2ml CHAM-NE mixed with MTC (1mg/kg), respectively.Results:The in vitro results indicated that CHAM-NE could potentiate the effect of MTC in sub-effective concentrations since the half-maximal inhibitory concentration (IC50) was reduced by a factor of 21.94 when compared to the MTC-NS. The in vivo study revealed that mice treated with CHAM-MTC showed a significant increase in the median survival time (MST= 37 days) when compared to the MTC-NS treated group (MST= 29.50 days). In addition, CHAM-MTC showed protective ability against the oxidative stress and hepatic damage induced by EAC and MTC treatment.Conclusion:The combination of MTC with CHAM-NE could be valuable in enhancing the therapeutic efficacy of MTC against EAC and in eliminating MTC-induced hepatotoxicity.

scholarly journals The in Vitro Effect of Polyvinylpyrrolidone and Citrate Coated Silver Nanoparticles on Erythrocytic Oxidative Damage and Eryptosis

2018 ◽  
Vol 49 (4) ◽  
pp. 1577-1588 ◽  
Author(s):  
Zannatul Ferdous ◽  
Sumaya Beegam ◽  
Saeed Tariq ◽  
Badreldin H Ali ◽  
Abderrahim Nemmar
Keyword(s):  
Oxidative Stress ◽  
Silver Nanoparticles ◽  
Antimicrobial Agents ◽  
Annexin V ◽  
Drug Carriers ◽  
Cellular Protein ◽  
Dependent Manner ◽  
Vitro Effect ◽  
Dose Dependent

Background/Aims: Silver nanoparticles (AgNPs) are increasingly used as antimicrobial agents and drug carriers in various biomedical fields. AgNPs can encounter erythrocytes either directly following intravenous injection, or indirectly via translocation from the site of administration. However, information regarding the pathophysiological effects and possible mechanism of action of AgNPs on the erythrocytes are still inadequately studied. Thus, the aim of our study was to investigate the mechanism underlying the effect of coating and concentration of AgNPs on mouse erythrocytes in vitro. Methods: We studied the interaction of polyvinylpyrrolidone (PVP) and citrate (CT) coated AgNPs (10 nm) at various concentrations (2.5, 10, 40 µg/ml) with mouse erythrocytes in vitro using various techniques including transmission electron microscopy (TEM), hemolysis, and colorimetric measurement of markers of oxidative stress comprising malondialdehyde (MDA), reduced glutathione (GSH), and catalase (CAT). Intracellular calcium (Ca2+) was determined using Fura 2AM fluorescence. Annexin V was quantified using ELISA and the caspase 3 was determined both flurometrically and by western blot technique. Results: Following incubation of the erythrocytes with AgNPs, both PVP- and CT- AgNPs induced significant and dose - dependent increase in hemolysis. TEM revealed that both PVP- and CT- AgNPs were taken up by erythrocytes. The erythrocyte susceptibility to lipid peroxidation measured by MDA was significantly increased in both PVP-and CT- AgNPs. The concentration of GSH and CAT activity were significantly decreased by both types of AgNPs. Additionally, PVP- and CT- AgNPs significantly increased intracellular Ca2+ in a dose -dependent manner. Likewise, the concentration of the cellular protein annexin V was significantly and dose - dependently enhanced by both types of AgNPs. Furthermore, PVP- and CT- AgNPs induced significant increase in calpain activity in incubated erythrocytes. Conclusion: We conclude that both PVP- and CT- AgNPs causes hemolysis, and are taken up by erythrocytes. Moreover, we demonstrated that AgNPs induces oxidative stress and eryptosis. These findings provide evidence for the potential pathophysiological effect of PVP-and CT- AgNPs on erythrocyte physiology.

Biogenic silver nanoparticles: In vitro and in vivo antitumor activity in bladder cancer

2020 ◽  
Vol 151 ◽  
pp. 162-170 ◽  
Author(s):  
Luiz Alberto Bandeira Ferreira ◽  
Fernanda Garcia-Fossa ◽  
Allan Radaic ◽  
Nelson Durán ◽  
Wagner José Fávaro ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Silver Nanoparticles ◽  
Antitumor Activity ◽  
Biogenic Silver Nanoparticles ◽  
In Vivo Antitumor Activity

Abstract MP231: Long Non-coding Rna Camirt Plays A Sentinel Role In Aging-related Heart Failure Via Interaction With Phb2 To Modulate Mitophagy Signaling In The Heart

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Xiao-Liang Wang ◽  
XIUCHUN LI ◽  
Hannah L Ong ◽  
Jae-Kyun Ko ◽  
Nuo Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Rna Binding ◽  
Physiological Role ◽  
Natural Aging ◽  
Annexin V ◽  
In Vitro Study ◽  
Live Cells ◽  
Mitochondrial Morphology

Background: Mitochondrial dysfunction is an important risk factor for heart failure in elderly people. Mitophagy, a physiological process that controls the removal of damaged mitochondria, is compromised in aging or failing hearts. In this study, we examined the physiological role of a cardiac-specific lncRNA Camirt that can potentially modulate mitophagy in the heart. Methods and Results: RNA-seq analysis and RT-PCR reveal a lncRNA is highly expressed in both mouse and human hearts, with undetectable levels in other vital organs. Furthermore, Real time qPCR was used to examine the expression of lncRNA in different animal models and in human hearts, which results showed that the expression of this lncRNA is decreased in aging mouse and human hearts, and failing mouse hearts induced by isoproterenol and doxorubicin. RNA pull-down and RNA-binding protein immunoprecipitation assays identify prohibitin-2 (Phb2), a known mitophagy receptor, as a binding partner for this lncRNA. Thus, we name this novel lncRNA as a cardiac-specific mitophagy-associated RNA transcript (Camirt). Camirt conditional (flox) knockout mice were created via CRISPR /Cas9 technology, and subjected to the longitudinal echocardiographic and survival studies. Mice with cardiac specific deletion of Camirt (Camirt-cKO) display progressive heart failure and die within 12 month after birth. RNA sequencing and gene ontology analysis revealed that genes involved in mitophagy signaling were significantly altered in the Camirt-cKO hearts compared with the littermate wild type mice. Transmission electron microscopy were used to examine the mitochondrial morphology in mouse hearts, and reveal excessive accumulation of mitolysosomes in cardiomyocytes derived from the Camirt-cKO mice. In vitro study with Annexin-V/PI staining showed an increased number of live cells and decreased number of apoptotic cells in cultured neonatal cardiomyocytes with overexpression of Camirt following oxidative stress induced by treatment with H2O2. Increased autophagy (or mitophagy) activity was observed in HL-1 cells with stable overexpression of Camirt and in the presence of chloroquine (an inhibitor for the lysosome degradation). While reduced Camirt expression via shRNA knock-down leads to compromised mitophagy activity in HL-1 cells. Further biochemical studies support the function of Camirt/Phb2 in maintenance of mitochondria function and mitophagy signaling under stress conditions. Conclusion: Overall, our results suggested that Camirt plays a sentinel role in aging-related heart failure via interaction with Phb2 to modulate mitophagy signaling in the heart. Future studies will focus on elucidating the in vivo role and mechanisms of Camirt in modulation of mitophagy under natural aging or stress-induced pathologic conditions using the loss- or gain-of-function of Camirt mouse models.

scholarly journals Somatostatin Receptors 2 and 5 Are the Major Somatostatin Receptors in Insulinomas: An in Vivo and in Vitro Study

2003 ◽  
Vol 88 (11) ◽  
pp. 5353-5360 ◽  
Author(s):  
J. Bertherat ◽  
F. Tenenbaum ◽  
K. Perlemoine ◽  
C. Videau ◽  
J. L. Alberini ◽  
...  
Keyword(s):  
Malignant Tumors ◽  
Specific Binding ◽  
Somatostatin Receptors ◽  
In Vitro Study ◽  
Scintigraphic Imaging ◽  
Cell Dysfunction ◽  
Receptor Scintigraphy ◽  
Displacement Experiments

Abstract Somatostatin (SRIF) receptors (sst) are present on normal pancreatic endocrine β-cells. However, the use of SRIF analogs in the scintigraphic imaging of insulinomas and in the medical management of these tumors seems to be restricted to a subgroup of patients. The aim of this study was to determine the prevalence of sst expression in vitro and characterize sst subtype binding in insulinomas and its correlation with in vivo sst receptor scintigraphy (SRS). In vitro studies were performed on 27 insulinomas from 25 patients: 22 with benign and three with malignant tumors. Semiquantitative RT-PCR of sst mRNAs was performed for 20 of these insulinomas. Sst2 and sst5 were expressed in 70%, sst1 in 50%, and sst3 and sst4 subtypes only in 15–20% of the tumors. 125I-Tyr0DTrp8SRIF14 binding was assessed by quantitative autoradiography in 18 insulinomas, and competition experiments were performed with SRIF14 and L797–591, L779–976, L796–778, L803–087, L817–818, selective agonists of the five sst subtypes, and BIM23244, a selective agonist of sst2 and sst5. Significant specific binding was observed in 72% of the insulinomas. Displacement experiments with ligands of higher affinity for each of the sst receptors revealed significant binding with the sst2 and sst5 ligands in 72%, sst3 in 44%, sst1 in 44%, and sst4 in 28% of cases. All insulinomas displaying sst2 binding were also sst5 sensitive. However, the ratio of sst5/sst2 displacement was variable and only equal to that for SRIF14 in experiments with the sst2/sst5 agonist BIM23244. SRS was performed 10 times in nine patients; it detected 60% of the tumors, including metastases of a malignant insulinoma. All the tumors detected by SRS displayed high levels of 125I-Tyr0DTrp8SRIF14 binding. The mechanisms underlying the loss of expression of sst2/sst5 in a third of insulinomas remains to be determined, but this loss of expression may be involved in β-cell dysfunction.

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