Preparation of a polymer-modified folate-targeted magnetic nano-delivery system and its inhibitory effect on nasopharyngeal carcinoma

2020 ◽  
Vol 10 (8) ◽  
pp. 1224-1229
Author(s):  
Shihong Yao ◽  
Pu Huang ◽  
Fen Liu ◽  
Fanyang Zeng ◽  
Wenxuan Zeng ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Delivery System ◽  
Caspase 3 ◽  
Inhibitory Effect ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Concentration Dependent Manner ◽  
Mtt Method ◽  
Pcr Method

The aims of this work were to investigate the effect of a polymer-modified folate-targeted magnetic nano-delivery system on growth inhibition of CNE2 cells and expression of Caspase-3 mRNA, and Caspase-3, Caspase-8, and Caspase-9 proteins, and to explore the mechanism used by this nano-delivery system to inhibit proliferation and induce apoptosis of human nasopharyngeal carcinoma cells. The MTT method was used to detect the effect of the polymer-modified folate-targeted magnetic nano-delivery system at different concentrations (0, 0.25, 0.50, 0.75, 1.00, 1.50, 2.00 g/mL) on CNE2 cell proliferation; the fluorescence PCR method was used to detect changes in Caspase-3 mRNA at different concentrations (0, 0.75, 1.00, 1.50 g/mL); and western blotting was used to detect Caspase-3, Caspase-8, and Caspase-9 expression. The polymer-modified folate-targeted magnetic nanoparticles inhibited the expression of Caspase-3 mRNA, and of Caspase-3, Caspase-8, and Caspase-9 in CNE2 cells in a concentration-dependent manner. It may be concluded that the polymer-modified folate-targeted magnetic nano-delivery system can inhibit the growth of CNE2 cells and its effect is closely related to the upregulation of Caspase-3 mRNA and Caspase-3, Caspase-8, and Caspase-9 protein expression and initiation of the caspase cascade.

scholarly journals Bullatacin Triggered ABCB1-Overexpressing Cell Apoptosis via the Mitochondrial-Dependent Pathway

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Ju Liang ◽  
Xu Zhang ◽  
Chun-Ling Dai ◽  
Jian-Ye Zhang ◽  
Yan-Yan Yan ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Multidrug Resistant ◽  
Resistant Cell ◽  
Ros Generation ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Concentration Dependent Manner ◽  
Induced Apoptosis ◽  
Dependent Pathway

This paper was to explore bullatacin-mediated multidrug-resistant cell apoptosis at extremely low concentration. To investigate its precise mechanisms, the pathway of cell apoptosis induced by bullatacin was examined. Bullatacin causes an upregulation of ROS and a downregulation ofΔΨmin a concentration-dependent manner in ABCB1-overexpressing KBv200 cells. In addition, cleavers of caspase-9, caspase-3, and PARP were observed following the release of cytochrome c from mitochondria after bullatacin treatment. However, neither cleavage of caspase-8 nor change of expression level of bcl-2, bax and Fas was observed by the same treatment. Pretreating KBv200 cells with N-acetylcysteine, an antioxidant modulator, resulted in a significant reduction of ROS generation and cell apoptosis induced by bullatacin. Bullatacin-induced apoptosis was antagonized by z-LEHD-fmk, a caspase-9 inhibitor, but not by z-IETD-fmk, a caspase-8 inhibitor. These implied that apoptosis of KBv200 cells induced by bullatacin was associated with the mitochondria-dependent pathway that was limited to activation of apical caspase-9.

scholarly journals NeosedumosideIII induced Apoptosis of Human Hepatocellular Carcinoma HepG2 cells and SMMC-7721 Cells and Related Mechanism

2021 ◽  
Author(s):  
Xin-Yu Li ◽  
Xin Zhou ◽  
Yu- Liu ◽  
Feng Qiu ◽  
Qing-Qing Zhao
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Human Hepatocellular Carcinoma ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Induced Apoptosis

Abstract Purpose: NeosedumosideIII (Neo) is a megastigmanes and belongs to monocyclic sesquiterpenoids compound with antioxidant, anti-inflammatory and other pharmacological activities. In order to explore the anti-cancer effect and possible mechanism of Neo, the study examined the anti-proliferation and apoptosis effect of Neo against human hepatocellular carcinoma HepG2 cells and SMMC-772 cells and related mechanism in vitro. Methods ：The anti-proliferation effect of Neo was detected on HepG2 cells and SMMC-772 cells by MTT assay and IC50 with increasing dose and time. Cell cycle and apoptosis were detected by flow cytometer. The changes of Bcl-2, Bax, Caspase-3, Caspase-8 and Caspase-9 proteins were detected by western blotting.Results ：The results indicated that Neo could inhibited proliferation of HepG2 cells and SMMC-772 cells in vitro and promoted apoptosis, it significantly induced apoptosis of HepG2 cells and SMMC-772 cells arrested cell cycle at G0/G1 phase in a dose-dependent manner, reduce the expression of Bcl-2 protein, and increase the expression of Bax and Caspase-3, Caspase-8 and Caspase-9 proteins. Conclusion：Neo could inhibit proliferation and induce apoptosis of HepG2 cells and SMMC-7721 cells in vivo which suggested that it might be served as a promising candidate for the treatment of liver cancer.

Compressive Force Induces Osteoblast Apoptosis via Caspase-8

2006 ◽  
Vol 85 (3) ◽  
pp. 240-244 ◽  
Author(s):  
Y. Goga ◽  
M. Chiba ◽  
Y. Shimizu ◽  
H. Mitani
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Compressive Force ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Osteoblast Apoptosis

Periodontal remodeling during orthodontic tooth movement is a result of mechanical stresses. The application of excessive orthodontic force induces cell death. However, the nature of compressive force-induced cell death is unclear. We examined whether the in vitro application of continuous compressive force would induce apoptosis in human osteoblast-like cells (MG-63 cells), and investigated the mechanism by which apoptosis was initiated. The cells became aligned irregularly, and cell viability decreased, indicating that the compressive force caused cell death. According to the TUNEL analysis, the number of apoptotic cells increased significantly in a time-and force-dependent manner. Caspase-3 activity increased with the magnitude of the compressive force, and this effect was reduced significantly by a caspase-8 inhibitor, whereas a caspase-9 inhibitor had no such effect. We conclude that the in vitro application of compressive force can induce apoptosis in MG-63 cells through the activation of caspase-3 via the caspase-8 signaling cascade.

scholarly journals Chemopreventive Effects and Antioxidant Capacity of Combined Leaf Extracts of Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus on Rhabdomyosarcoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Clayton E. Siamayuwa ◽  
Loveness K. Nyanga ◽  
Cathrine Chidewe
Keyword(s):  
Antioxidant Capacity ◽  
Cell Line ◽  
Caspase 3 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Leaf Extracts ◽  
Concentration Dependent Manner ◽  
Rd Cells ◽  
Antioxidant Capacity Assays ◽  
Increased Activity

Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus contain compounds that have antimutagenic properties. The rise in rhabdomyosarcoma in paediatrics and prognosis of the disease in infants compared to adults calls for newer, less toxic alternatives in treatment of the disease. The aim of this study was to determine the anticancer activity and antioxidant capacity of combined leaf extracts of Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus (SAHA), against rhabdomyosarcoma (RMS) using rhabdomyosarcoma (RD) cell line and mouse (L20B) cell line. Cytotoxicity, morphology, apoptosis induction, and antioxidant capacity assays were done. Of the four solvents used for extraction, the dichloromethane SAHA extract was the most cytotoxic with IC50 of 106 μg/mL after doxorubicin, the reference anticancer drug with IC50 of 0.8 μg/mL. The SAHA extracts had a stronger cytotoxicity effect on the cancerous RD cells than on normal L20B cells. Morphological assessment showed untreated cells maintained their normal striated appearance of muscle cells whereas cells treated with doxorubicin or SAHA extracts exhibited cell shrinkage, loss of surface adherence, reduced cell density along with cell debris, which is a characteristic of apoptosis. Normal L20B cells when treated with doxorubicin or SAHA extracts, maintained their cell shape, and remained adherent to the surface. The apoptotic enzyme caspase-3 was induced in a concentration dependent manner upon treatment of the RD cells with SAHA extracts or doxorubicin. Induction of caspase-3 was ten times less in treated L20B cells compared to the RD cells. Low induction of caspase-9 enzyme was observed in both treated RD and L20B cells. Treatment of both RD and L20B cells with SAHA extracts or doxorubicin resulted in increased activity of peroxidase and reduction of oxidative stress. Results of the study show that the SAHA extracts are potential sources of compounds that may serve as useful agents for treatment of rhabdomyosarcoma.

scholarly journals Japanese encephalitis virus infection activates caspase-8 and -9 in a FADD-independent and mitochondrion-dependent manner

2008 ◽  
Vol 89 (8) ◽  
pp. 1930-1941 ◽  
Author(s):  
Chang-Huei Tsao ◽  
Hong-Lin Su ◽  
Yi-Ling Lin ◽  
Han-Pang Yu ◽  
Shu-Ming Kuo ◽  
...  
Keyword(s):  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Caspase 3 ◽  
Encephalitis Virus ◽  
Dominant Negative Mutant ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Effector Caspase ◽  
Induced Apoptosis

Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, replicates primarily at the endoplasmic reticulum and thereby triggers apoptosis of infected cells. This study investigated the hierarchical activation of the caspase network induced by JEV infection. It was found that JEV activated the initiators caspase-8 and -9, as well as effector caspase-3, in infected baby hamster kidney and mouse neuroblastoma (N18) cells. In neuronal N18 cells, JEV infection triggered cytochrome c release from mitochondria, which in turn activated caspase-9 and -3. Treatment of JEV-infected N18 cells with cyclosporin A or ruthenium red, which attenuate mitochondrial injuries, blocked activation of caspase-9 or -3, typifying that, in neuronal cells, this apoptosis involves the mitochondrial pathway. Alternatively, in caspase-3-deficient MCF-7 cells, JEV persisted and readily triggered a typical apoptotic response, including cytochrome c release and full activation of caspase-9 and -8 along with caspase-6, indicating that JEV did not require caspase-3 to manifest caspase-8 activation and apoptosis. Interestingly, a Fas-associated death-domain-containing protein (FADD) dominant-negative mutant, which interfered with transmission of the extracellular death signals into cells through the Fas/tumour necrosis factor (TNF) receptor, failed to block JEV-induced apoptosis and caspase-8 activation, implying that receptor oligomerization of the Fas/TNF pathway might not participate in JEV-induced apoptosis. Taken together, these results illustrate that JEV infection triggers caspase cascades involving the initiators caspase-8 and -9, probably through FADD-independent but mitochondrion-dependent pathways.

scholarly journals Meisoindigo inhibits cellular proliferation via down-regulation of the PI3K/Akt pathway and induces cellular apoptosis in glioblastoma U87 cells

2021 ◽  
Author(s):  
Lijuan Gu ◽  
Yi Zhou ◽  
Yingze Ye ◽  
Xiqun Zhu ◽  
Tong Jin ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Cellular Proliferation ◽  
Nuclear Translocation ◽  
Morphological Changes ◽  
Inhibitory Effect ◽  
Cell Counting ◽  
Akt Pathway ◽  
Dependent Manner ◽  
Caspase 9 ◽  
U87 Cells

Objective: The current study was to explore whether meisoindigo was effective in suppressing proliferation and inducing apoptosis of human glioblastoma multiforme U87 cells and to explore its possible mechanisms. Method: Morphological changes were observed by light microscopy. Cell counting kit-8 (CCK-8) assay was performed to detect cellular proliferation. Apoptosis was monitored by flow cytometry. Akt, phospho-Akt, PI3K, p65, phospho-p65 and apoptosis-related proteins caspase-3 and caspase-9 were examined by Western blotting assays. Immunofluorescence was used to evaluate level of P65 expression in cells. Result: Meisoindigo inhibited the proliferation of U87 cells, and the inhibitory effect increased in a dose dependent manner. Moreover, meisoindigo exposure triggered an increase in the level of caspase-3 and caspase-9, supporting its role in the activation of apoptosis. Furthermore, meisoindigo reduced the expression of PI3K, Akt, phospho-Akt, NF-κB, p65 and phospho-p65 in U87 cells, and displacement of p65 from the nucleus to the cytoplasm. Conclusion: Meisoindigo inhibits proliferation and induces apoptosis of U87 cells, probably through down-regulating the PI3K/Akt pathway and reducing nuclear translocation of NF-κB p65.

Phenyhexyl Isothiocyanate, a Dual Inhibitor of Histone Deacetylation and Methylation, Inhibit Acute Lymphoblastic Leukemia Cells through Epigenetic Modulation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4532-4532
Author(s):  
Yiqun Huang ◽  
Xudong Ma ◽  
Dicky J.W. Chiao ◽  
Delong Liu
Keyword(s):  
Cell Cycle ◽  
Acute Lymphoblastic Leukemia ◽  
Caspase 3 ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Dual Inhibitor

Abstract We have shown that phenyhexyl isothiocyanate(PHI) is a novel histone deacetylase inhibitor and can also modulate histone methylation. In this study we investigated the effect of PHI on human Acute Lymphoblastic leukemia cell line Molt-4 in vitro. The viability of Molt-4 cells was determined by MTT method. Apoptosis and cell cycle arrest were measured by flow cytometry. The expression of bcl-2, caspase-9, caspase-8, caspase-3, PRAP protein, acetylated H3 and H4, methylated H3K9 and H3K4 were detected by Western Blotting. The results showed that PHI inhibited the cell growth and decreased viability of Molt-4 cells. Cell cycle analysis indicated an arrest in G0/G1 phase. The expression of bcl-2, caspase-9, caspase-3, and PRAP was inhibited by PHI in a dose and time dependent manner. In contrast, there was no significant change in the expression of Caspase-8. PHI also significantly increased the level of acetylated histone H3 as well as H4. Interestingly, PHI increased the level of methylated H3k4, but decreased methylated H3K9. These data suggest that ALL cells are sensitive to the novel HDAC inhibitor, and PHI may become a novel agent in ALL therapy.

scholarly journals Leptospira interrogans Induces Apoptosis in Macrophages via Caspase-8- and Caspase-3-Dependent Pathways

2008 ◽  
Vol 77 (2) ◽  
pp. 799-809 ◽  
Author(s):  
Dandan Jin ◽  
David M. Ojcius ◽  
Dexter Sun ◽  
Haiyan Dong ◽  
Yihui Luo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Host Cells ◽  
Caspase 8 ◽  
Lamin A ◽  
Leptospira Interrogans ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Caspase 6 ◽  
Induced Apoptosis

ABSTRACT Apoptosis of host cells plays an important role in modulating the pathogenesis of many infectious diseases. It has been reported that Leptospira interrogans, the causal agent of leptospirosis, induces apoptosis in macrophages and hepatocytes. However, the molecular mechanisms responsible for host cell death remained largely unknown. Here we demonstrate that L. interrogans induced apoptosis in a macrophage-like cell line, J774A.1, and primary murine macrophages in a time- and dose-dependent manner. Apoptosis was associated with the activation of cysteine aspartic acid-specific proteases (caspase-3, caspase-6, and caspase-8), the increased expression of Fas-associated death domain (FADD), and the cleavage of the caspase substrates poly(ADP-ribose) polymerase (PARP) and nuclear lamina protein (lamin A and lamin C). Caspase-9 was activated to a lesser extent, whereas no release of cytochrome c from mitochondria was detectable. Inhibition of caspase-8 impaired L. interrogans-induced caspase-3 and -6 activation, as well as PARP and lamin A/C cleavage and apoptosis, suggesting that apoptosis is initiated via caspase-8 activation. Furthermore, caspase-3 was required for the activation of caspase-6 and seemed to be involved in caspase-9 activation through a feedback amplification loop. These data indicate that L. interrogans-induced apoptosis in macrophages is mediated by caspase-3 and -6 activation through a FADD-caspase-8-dependent pathway, independently of mitochondrial cytochrome c-caspase-9-dependent signaling.

scholarly journals Brassinolide Enhances the Level of Brassinosteroids, Protein, Pigments, and Monosaccharides in Wolffia arrhiza Treated with Brassinazole

Plants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1311
Author(s):  
Magdalena Chmur ◽  
Andrzej Bajguz
Keyword(s):  
Plant Growth ◽  
Growth And Development ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Plant Growth And Development ◽  
Concentration Dependent Manner ◽  
Spectrophotometric Methods ◽  
Synthetic Inhibitor ◽  
Wolffia Arrhiza ◽  
First Time

Brassinolide (BL) represents brassinosteroids (BRs)—a group of phytohormones that are essential for plant growth and development. Brassinazole (Brz) is as a synthetic inhibitor of BRs’ biosynthesis. In the present study, the responses of Wolffia arrhiza to the treatment with BL, Brz, and the combination of BL with Brz were analyzed. The analysis of BRs and Brz was performed using LC-MS/MS. The photosynthetic pigments (chlorophylls, carotenes, and xanthophylls) levels were determined using HPLC, but protein and monosaccharides level using spectrophotometric methods. The obtained results indicated that BL and Brz influence W. arrhiza cultures in a concentration-dependent manner. The most stimulatory effects on the growth, level of BRs (BL, 24-epibrassinolide, 28-homobrassinolide, 28-norbrassinolide, catasterone, castasterone, 24-epicastasterone, typhasterol, and 6-deoxytyphasterol), and the content of pigments, protein, and monosaccharides, were observed in plants treated with 0.1 µM BL. Whereas the application of 1 µM and 10 µM Brz caused a significant decrease in duckweed weight and level of targeted compounds. Application of BL caused the mitigation of the Brz inhibitory effect and enhanced the BR level in duckweed treated with Brz. The level of BRs was reported for the first time in duckweed treated with BL and/or Brz.

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