Displaying publications 41 - 60 of 192 in total

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  1. Fulltext Targeted Photodynamic Therapy using a Vectorized Photosensitizer coupled to Folic Acid Analog induces Ovarian Tumor Cell Death and inhibits IL-6-mediated Inflammation
    Boidin L, Moinard M, Moussaron A, Merlier M, Moralès O, Grolez GP, et al.
    J Control Release, 2024 Jul;371:351-370.
    PMID: 38789088 DOI: 10.1016/j.jconrel.2024.05.033
    Ovarian cancer (OC) is one of the most lethal cancers among women. Frequent recurrence in the peritoneum due to the presence of microscopic tumor residues justifies the development of new therapies. Indeed, our main objective is to develop a targeted photodynamic therapy (PDT) treatment of peritoneal carcinomatosis from OC to improve the life expectancy of cancer patients. Herein, we propose a targeted-PDT using a vectorized photosensitizer (PS) coupled with a newly folic acid analog (FAA), named PSFAA, in order to target folate receptor alpha (FRα) overexpressed on peritoneal metastasis. This PSFAA was the result of the coupling of pyropheophorbide-a (Pyro-a), as the PS, to a newly synthesized FAA via a polyethylene glycol (PEG) spacer. The selectivity and the PDT efficacy of PSFAA was evaluated on two human OC cell lines overexpressing FRα compared to fibrosarcoma cells underexpressing FRα. Final PSFAA, including the synthesis of a newly FAA and its conjugation to Pyro-a, was obtained after 10 synthesis steps, with an overall yield of 19%. Photophysical properties of PSFAA in EtOH were performed and showed similarity with those of free Pyro-a, such as the fluorescence and singlet oxygen quantum yields (Φf = 0.39 and ΦΔ = 0.53 for free Pyro-a, and Φf = 0.26 and ΦΔ = 0.41 for PSFAA). Any toxicity of PSFAA was noticed. After light illumination, a dose-dependent effect on PS concentration and light dose was shown. Furthermore, a PDT efficacy of PSFAA on OC cell secretome was detected inducing a decrease of a pro-inflammatory cytokine secretion (IL-6). This new PSFAA has shown promising biological properties highlighting the selectivity of the therapy opening new perspectives in the treatment of a cancer in a therapeutic impasse.
    Matched MeSH terms: Cell Death/drug effects
  2. Fulltext Anticancer Drug Discovery from Microbial Sources: The Unique Mangrove Streptomycetes
    Law JW, Law LN, Letchumanan V, Tan LT, Wong SH, Chan KG, et al.
    Molecules, 2020 Nov 17;25(22).
    PMID: 33212836 DOI: 10.3390/molecules25225365
    Worldwide cancer incidence and mortality have always been a concern to the community. The cancer mortality rate has generally declined over the years; however, there is still an increased mortality rate in poorer countries that receives considerable attention from healthcare professionals. This suggested the importance of the prompt detection, effective treatment, and prevention strategies. The genus Streptomyces has been documented as a prolific producer of biologically active secondary metabolites. Streptomycetes from mangrove environments attract researchers' attention due to their ability to synthesize diverse, interesting bioactive metabolites. The present review highlights research on mangrove-derived streptomycetes and the production of anticancer-related compounds from these microorganisms. Research studies conducted between 2008 and 2019, specifically mentioning the isolation of streptomycetes from mangrove areas and described the successful purification of compound(s) or generation of crude extracts with cytotoxic activity against human cancer cell lines, were compiled in this review. It is anticipated that there will be an increase in prospects for mangrove-derived streptomycetes as one of the natural resources for the isolation of chemotherapeutic agents.
    Matched MeSH terms: Cell Death/drug effects
  3. Metal Oxide Nanoparticles Exhibit Anti-Acanthamoeba castellanii Properties by Inducing Necrotic Cell Death
    Ahmed U, Gew LT, Siddiqui R, Khan NA, Alharbi AM, Alhazmi A, et al.
    Acta Parasitol, 2024 Sep;69(3):1717-1723.
    PMID: 39153011 DOI: 10.1007/s11686-024-00891-2
    PURPOSE: The treatment of amoebic infections is often problematic, largely due to delayed diagnosis, amoebae transformation into resistant cyst form, and lack of availability of effective chemotherapeutic agents. Herein, we determined anti-Acanthamoeba castellanii properties of three metal oxide nanoparticles (TiO2, ZrO2, and Al2O3).

    METHODS: Amoebicidal assays were performed to determine whether metal oxide nanoparticles inhibit amoebae viability. Encystation assays were performed to test whether metal oxide nanoparticles inhibit cyst formation. By measuring lactate dehydrogenase release, cytotoxicity assays were performed to determine human cell damage. Hoechst 33342/PI staining was performed to determine programmed cell death (apoptosis) and necrosis in A. castellanii.

    RESULTS: TiO2-NPs significantly inhibited amoebae viability as observed through amoebicidal assays, as well as inhibited their phenotypic transformation as evident using encystation assays, and showed limited human cell damage as observed by measuring lactate dehydrogenase assays. Furthermore, TiO2-NPs altered parasite membranes and resulted in necrotic cell death as determined using double staining cell death assays with Hoechst33342/Propidium iodide (PI) observed through chromatin condensation. These findings suggest that TiO2-NPs offers a potential viable avenue in the rationale development of therapeutic interventions against Acanthamoeba infections.

    Matched MeSH terms: Cell Death/drug effects
  4. Identification and validation of mRNA profiles linked to ATP- induced cell death represent a novel prognostic model for breast cancer
    Zhang Z, Zhang H, Zhang Z, Sandai D, Lu P, Zhang H, et al.
    Front Immunol, 2024;15:1483498.
    PMID: 39555060 DOI: 10.3389/fimmu.2024.1483498
    BACKGROUND: Cell death mechanisms are integral to the pathogenesis of breast cancer (BC), with ATP-induced cell death (AICD) attracting increasing attention due to its distinctive specificity and potential therapeutic applications.

    METHODS: This study employed genomic methodologies to investigate the correlation between drug sensitivity and types of AICD in BC. Initially, data from TCGA were utilized to construct a prognostic model and classification system for AICD. Subsequently, a series of bioinformatics analyses assessed the prognostic and clinical significance of this model within the context of BC.

    RESULTS: Analysis revealed a cohort of 18 genes associated with AICD, exhibiting prognostic relevance. Survival analyses indicated that overall survival rates were significantly lower in high-risk populations compared to their low-risk counterparts. Furthermore, prognostic indicators linked to AICD demonstrated high accuracy in predicting survival outcomes in BC. Immunological assessments indicated heightened expression of anti-tumor infiltrating immune cells and immune checkpoint molecules in low-risk populations, correlating with various anti-tumor immune functions. Ultimately, a comprehensive prognostic model related to AICD was developed through univariate analysis, least absolute shrinkage and selection operator (LASSO), and multivariate Cox regression analysis. As Adenosine triphosphate (ATP) concentration increased, the viability of BC cells exhibited a general decline at each time point. Notably, ATP diminished the mitochondrial membrane potential in BC cells while enhancing it in normal breast epithelial cells. Additionally, ATP inhibited the migration of BC cells and promoted their apoptosis. ATP also stimulated reactive oxygen species (ROS) production in MCF-10A cells, with implications for the immune response in BC cells. Compared to the control group, expression levels of CLIC6, SLC1A1, and CEMIP were significantly reduced in the ATP intervention group, whereas ANO6 expression was elevated. ANO6, CEMIP, and CLIC6 share genetic variants with BC, while SLC1A1 does not exhibit genetic causal variation with the disease.

    CONCLUSION: A valuable prognostic model associated with AICD has been established, capable of accurately predicting BC prognosis. The induction of cell death by ATP appears to play a protective role in BC progression. These findings carry significant implications for the implementation of personalized and tailored treatment strategies for BC patients.

    Matched MeSH terms: Cell Death/genetics
  5. The cathepsin B inhibitor, z-FA-CMK is toxic and readily induced cell death in human T lymphocytes
    Liow KY, Chow SC
    Toxicol Appl Pharmacol, 2013 Nov 1;272(3):559-67.
    PMID: 23933532 DOI: 10.1016/j.taap.2013.07.022
    The cathepsin B inhibitor, benzyloxycarbonyl-phenylalanine-alanine-chloromethylketone (z-FA-CMK) was found to be toxic and readily induced cell death in the human T cell line, Jurkat, whereas two other analogs benzyloxycarbonyl-phenylalanine-alanine-fluoromethylketone (z-FA-FMK) and benzyloxycarbonyl-phenylalanine-alanine-diazomethylketone (z-FA-DMK) were not toxic. The toxicity of z-FA-CMK requires not only the CMK group, but also the presence of alanine in the P1 position and the benzyloxycarbonyl group at the N-terminal. Dose-response studies showed that lower concentrations of z-FA-CMK induced apoptosis in Jurkat T cells whereas higher concentrations induced necrosis. In z-FA-CMK-induced apoptosis, both initiator caspases (-8 and -9) and effector caspases (-3, -6 and -7) were processed to their respective subunits in Jurkat T cells. However, only the pro-form of the initiator caspases were reduced in z-FA-CMK-induced necrosis and no respective subunits were apparent. The caspase inihibitor benzyloxycarbonyl-valine-alanine-aspartic acid-(O-methyl)-fluoromehylketone (z-VAD-FMK) inhibits apoptosis and caspase processing in Jurkat T cells treated with low concentration of z-FA-CMK but has no effect on z-FA-CMK-induced necrosis and the loss of initiator caspases. This suggests that the loss of initiator caspases in Jurkat T cells during z-FA-CMK-induced necrosis is not a caspase-dependent process. Taken together, we have demonstrated that z-FA-CMK is toxic to Jurkat T cells and induces apoptosis at low concentrations, while at higher concentrations the cells die of necrosis.
    Matched MeSH terms: Cell Death/drug effects; Cell Death/physiology
  6. Fulltext Complement-Opsonized HIV-1 Alters Cross Talk Between Dendritic Cells and Natural Killer (NK) Cells to Inhibit NK Killing and to Upregulate PD-1, CXCR3, and CCR4 on T Cells
    Ellegård R, Khalid M, Svanberg C, Holgersson H, Thorén Y, Wittgren MK, et al.
    Front Immunol, 2018;9:899.
    PMID: 29760706 DOI: 10.3389/fimmu.2018.00899
    Dendritic cells (DCs), natural killer (NK) cells, and T cells play critical roles during primary HIV-1 exposure at the mucosa, where the viral particles become coated with complement fragments and mucosa-associated antibodies. The microenvironment together with subsequent interactions between these cells and HIV at the mucosal site of infection will determine the quality of immune response that ensues adaptive activation. Here, we investigated how complement and immunoglobulin opsonization influences the responses triggered in DCs and NK cells, how this affects their cross talk, and what T cell phenotypes are induced to expand following the interaction. Our results showed that DCs exposed to complement-opsonized HIV (C-HIV) were less mature and had a poor ability to trigger IFN-driven NK cell activation. In addition, when the DCs were exposed to C-HIV, the cytotolytic potentials of both NK cells and CD8 T cells were markedly suppressed. The expression of PD-1 as well as co-expression of negative immune checkpoints TIM-3 and LAG-3 on PD-1 positive cells were increased on both CD4 as well as CD8 T cells upon interaction with and priming by NK-DC cross talk cultures exposed to C-HIV. In addition, stimulation by NK-DC cross talk cultures exposed to C-HIV led to the upregulation of CD38, CXCR3, and CCR4 on T cells. Together, the immune modulation induced during the presence of complement on viral surfaces is likely to favor HIV establishment, dissemination, and viral pathogenesis.
    Matched MeSH terms: Programmed Cell Death 1 Receptor/biosynthesis; Programmed Cell Death 1 Receptor/immunology
  7. A novel antiamoebic agent against Acanthamoeba sp.--A causative agent for eye keratitis infection
    Kusrini E, Hashim F, Azmi WN, Amin NM, Estuningtyas A
    Spectrochim Acta A Mol Biomol Spectrosc, 2016 Jan 15;153:714-21.
    PMID: 26474244 DOI: 10.1016/j.saa.2015.09.021
    The terbium trinitrate.trihydrate.18-crown ether-6, Tb(NO3)3(OH2)3.(18C6) complex has been characterized by elemental analysis, photoluminescence and single X-ray diffraction. The IC50 values were determined based on MTT assay while light and fluorescence microscopy imaging were employed to evaluate the cellular morphological changes. Alkaline comet assay was performed to analyze the DNA damage. The photoluminescence spectrum of the Tb complex excited at 325 nm displayed seven luminescence peaks corresponding to the (5)D4→(7)F(0, 1, 2, 3, 4, 5, 6) transitions. The cytotoxicity and genotoxicity studies indicated that the Tb(NO3)3(OH2)3.(18C6) complex and its salt form as well as the 18C6 molecule have excellent anti-amoebic activity with very low IC50 values are 7, 2.6 and 1.2 μg/mL, respectively, with significant decrease (p<0.05) in Acanthamoeba viability when the concentration was increased from 0 to 30 μg/mL. The mode of cell death in Acanthamoeba cells following treatment with the Tb complex was apoptosis. This is in contrast to the Tb(NO3)3.6H2O salt- and 18C6 molecule-treated Acanthamoeba, which exhibited necrotic type cells. The percentage of DNA damage following treatment with all the compounds at the IC25 values showed high percentage of type 1 with the % nuclei damage are 14.15±2.4; 46.00±4.2; 36.36±2.4; 45.16±0.6%, respectively for untreated, treated with Tb complex, Tb salt and 18C6 molecule. The work features promising potential of Tb(NO3)3(OH2)3.(18C6) complex as anti-amoebic agent, representing a therapeutic option for Acanthamoeba keratitis infection.
    Matched MeSH terms: Cell Death
  8. Fulltext Ultra-structural changes and expression of chondrogenic and hypertrophic genes during chondrogenic differentiation of mesenchymal stromal cells in alginate beads
    Dashtdar H, Murali MR, Selvaratnam L, Balaji Raghavendran H, Suhaeb AM, Ahmad TS, et al.
    PeerJ, 2016;4:e1650.
    PMID: 26966647 DOI: 10.7717/peerj.1650
    Chondrogenic differentiation of mesenchymal stromal cells (MSCs) in the form of pellet culture and encapsulation in alginate beads has been widely used as conventional model for in vitro chondrogenesis. However, comparative characterization between differentiation, hypertrophic markers, cell adhesion molecule and ultrastructural changes during alginate and pellet culture has not been described. Hence, the present study was conducted comparing MSCs cultured in pellet and alginate beads with monolayer culture. qPCR was performed to assess the expression of chondrogenic, hypertrophic, and cell adhesion molecule genes, whereas transmission electron microscopy (TEM) was used to assess the ultrastructural changes. In addition, immunocytochemistry for Collagen type II and aggrecan and glycosaminoglycan (GAG) analysis were performed. Our results indicate that pellet and alginate bead cultures were necessary for chondrogenic differentiation of MSC. It also indicates that cultures using alginate bead demonstrated significantly higher (p < 0.05) chondrogenic but lower hypertrophic (p < 0.05) gene expressions as compared with pellet cultures. N-cadherin and N-CAM1 expression were up-regulated in second and third weeks of culture and were comparable between the alginate bead and pellet culture groups, respectively. TEM images demonstrated ultrastructural changes resembling cell death in pellet cultures. Our results indicate that using alginate beads, MSCs express higher chondrogenic but lower hypertrophic gene expression. Enhanced production of extracellular matrix and cell adhesion molecules was also observed in this group. These findings suggest that alginate bead culture may serve as a superior chondrogenic model, whereas pellet culture is more appropriate as a hypertrophic model of chondrogenesis.
    Matched MeSH terms: Cell Death
  9. Fulltext Aberrant expression of the S1P regulating enzymes, SPHK1 and SGPL1, contributes to a migratory phenotype in OSCC mediated through S1PR2
    Patmanathan SN, Johnson SP, Lai SL, Panja Bernam S, Lopes V, Wei W, et al.
    Sci Rep, 2016 05 10;6:25650.
    PMID: 27160553 DOI: 10.1038/srep25650
    Oral squamous cell carcinoma (OSCC) is a lethal disease with a 5-year mortality rate of around 50%. Molecular targeted therapies are not in routine use and novel therapeutic targets are required. Our previous microarray data indicated sphingosine 1-phosphate (S1P) metabolism and signalling was deregulated in OSCC. In this study, we have investigated the contribution of S1P signalling to the pathogenesis of OSCC. We show that the expression of the two major enzymes that regulate S1P levels were altered in OSCC: SPHK1 was significantly upregulated in OSCC tissues compared to normal oral mucosa and low levels of SGPL1 mRNA correlated with a worse overall survival. In in vitro studies, S1P enhanced the migration/invasion of OSCC cells and attenuated cisplatin-induced death. We also demonstrate that S1P receptor expression is deregulated in primary OSCCs and that S1PR2 is over-expressed in a subset of tumours, which in part mediates S1P-induced migration of OSCC cells. Lastly, we demonstrate that FTY720 induced significantly more apoptosis in OSCC cells compared to non-malignant cells and that FTY720 acted synergistically with cisplatin to induce cell death. Taken together, our data show that S1P signalling promotes tumour aggressiveness in OSCC and identify S1P signalling as a potential therapeutic target.
    Matched MeSH terms: Cell Death
  10. Prediction of colorectal cancer driver genes from patients’ genome data
    Muhammad-iqmal Abdullah, Nor Azlan Nor Muhammad
    Sains Malaysiana, 2018;47:3095-3105.
    Colorectal cancer refers to the cancer that occurs in the colon and rectum. It has been established as the third most
    common cancer and the forth one in causing worldwide mortality. Cancer caused by the mutation of several genes that
    usually involved in the regulation of cell proliferation, growth and cell death. The mutation that leads to abnormal
    function of genes, either in enabling the genes to gain or loss of function was termed as driver mutation and the genes
    with driver mutation ability was termed as driver genes. The identification of driver genes provides insight on mechanistic
    process of cancer development where this information can be used to further understand their mode of action for causing
    dysregulation in signaling pathways. In this study, two bioinformatic tools, i.e. CGI and iCAGES were used to predict
    potential driver genes from the genome of eight colorectal cancer patients with annotated variants datasets. 44 unique
    driver genes and 21 pathways have been identified; such as p53 signaling, PI3K-AKT, Endocrine resistance, MAPK and
    cell cycle pathways. The identification of these pathways can lead to the identification of potential drugs targeting these
    pathways.
    Matched MeSH terms: Cell Death
  11. Biomimetic amphiphilic chitosan nanoparticles: Synthesis, characterization and antimicrobial activity
    Ahmad N, Wee CE, Wai LK, Zin NM, Azmi F
    Carbohydr Polym, 2021 Feb 15;254:117299.
    PMID: 33357867 DOI: 10.1016/j.carbpol.2020.117299
    Naturally derived antimicrobial peptides (AMPs) are an attractive source of new antimicrobial agents. However, clinical application of AMPs is associated with poor bioavailability and toxicity. In this study, we address these limitations by designing a new series of chitosan derivatives to mimic the amphiphilic topology of AMPs. The synthesized chitosan derivatives were found to self-assemble into nanoparticles in the aqueous environment. Among the compounds, a chitosan derivative grafted with arginine and oleic acid (CH-Arg-OA) exhibited the most potent antimicrobial activity, especially against Gram-negative bacteria. It also caused minimal cell death when tested in HEK293 and HepG2 cell lines, thus confirming the role of cationicity and lipophilicity for selective bacteria targeting. CH-Arg-OA exhibited its antimicrobial activity by disrupting bacterial membranes and causing the leakage of cytoplasmic contents. Thus, amphiphilic chitosan nanoparticles offer a great promise as a new class of AMPs mimics that is effective against Gram-negative bacteria.
    Matched MeSH terms: Cell Death
  12. Fulltext Programmed cell death-ligand, thymidylate synthase and deleted in colorectal carcinoma biomarkers in colorectal carcinoma
    Fauzah Abd Ghani, Reena Rehavu Zin, Maha Abdullah, Norhafizah Mohtarrudin, Ebenyi Emeka Onwe
    Malaysian Journal of Medicine and Health Sciences, 2019;15(108):16-16.
    MyJurnal
    Introduction: It is well known that cancer cells evade the immune system with the help of programmed cell death protein 1 (PD-L1) molecule to remain undetected, causing abnormal proliferation of T-cells. PD-L1 expression on the surface of neoplastic cells inhibits cytotoxic T-cell responses which lead to negative regulation of cytokines and proliferation of T-cells. The deleted in colorectal cancer (DCC) gene belongs to the immunoglobulin superfamily. It is a candidate of the tumour suppressor gene by regulating apoptosis. DCC assessment gives an insight into progno-sis in patients with advanced stages of CRC. Thymidylate synthase (TYMS) is a highly conserved enzyme involved in DNA synthesis. TYMS has been an important target for cancer chemotherapy because of its central, rate-limiting role in de novo synthesis of thymidylate. Expression of PD-L1, TYMS and DCC has been demonstrated to confer a prognostic value in CRC but none have been completely validated for patient care. This study aimed to determine the prognostic and predictive potential of PD-L1, TYMS, and DCC biomarkers in CRC. Methods: The expression of these biomarkers was evaluated immunohistochemically in 91 formalin-fixed paraffin-embedded (FFPE) archival tumour samples from patients that underwent surgical resection. Results: There was high expression of DCC in most cases; 84.6% (77/91). TYMS expression at a high level score was 46.2% (42/91) and at low level was 53.8% (49/91). Majority of cases had low PD-L1 expression in 93.4% (86/91) cases and high expression was detected in 6.6% (6/94) of cases. In addition, there was a significant association between TYMS expression with gender (P < 0.05) with distribution of TYMS expression detected at high level was 76.2% in male and 23.8% in female. The Kaplan-Meier survival plot showed mean overall survival in patients with PD-L1 with high expression to be 22 months, which pre-dicts better survival. TYMS low expression showed mean overall survival of 90 which also indicated better survival. DCC high expression showed mean overall survival of 90 which indicated better survival. The correlation between the biomarkers and overall survival were not statistically significant. Conclusion: The results from this study suggest that PD-L1, TYMS and DCC expression could be used as biomarkers to predict treatment outcome in CRC. PD-L1 overexpression predicts patients who could benefit from anti-PD-1 and anti-PD-L1 immunotherapy whilst TYMS low expression predicts patients who could benefit from 5-fluorouracil therapy. DCC high expression tumours predicts a better prognosis and overall survival compared to DCC-negative tumours in advanced CRC.
    Matched MeSH terms: Programmed Cell Death 1 Receptor
  13. Fulltext Bystander Effect Induced in Breast Cancer (MCF-7) and Human Osteoblast Cell Lines (hFOB 1.19) with HDR-Brachytherapy
    Zainudin Nh M, R A, W N R
    J Biomed Phys Eng, 2020 Jun;10(3):319-328.
    PMID: 32637376 DOI: 10.31661/jbpe.v0i0.1135
    Background: Radiation induced bystander effects (RIBEs) occurs in unirradiated cells exhibiting indirect biological effect as a consequence of signals from other irradiated cells in the population.

    Objective: In this study, bystander effects in MCF-7 breast cancer cells and hFOB 1.19 normal osteoblast cells irradiated with gamma emitting HDR Brachytherapy Ir-192 source were investigated.

    Material and Methods: In this in-vitro study, bystander effect stimulation was conducted using medium transfer technique of irradiated cells to the non-irradiated bystander cells. Cell viability, reactive oxygen species (ROS) generation and colony forming assay was employed to evaluate the effect.

    Results: Results indicate that the exposure to the medium irradiated MCF-7 induced significant bystander killing and decreased the survival fraction of bystander MCF-7 and hFOB from 1.19 to 81.70 % and 65.44 %, respectively. A significant decrease in survival fraction was observed for hFOB 1.19 bystander cells (p < 0.05). We found that the rate of hFOB 1.19 cell growth significantly decreases to 85.5% when added with media from irradiated cells. The ROS levels of bystander cells for both cell lines were observed to have an increase even after 4 h of treatment. Our results suggest the presence of bystander effects in unirradiated cells exposed to the irradiated medium.

    Conclusion: These data provide evidence that irradiated MCF-7 breast cancer cells can induce bystander death in unirradiated MCF-7 and hFOB 1.19 bystander cells. Increase in cell death could also be mediated by the ROS generation during the irradiation with HDR brachytherapy.

    Matched MeSH terms: Cell Death
  14. Effect of Chitosan Nanoparticle-Loaded Thymus serpyllum on Hydrogen Peroxide-Induced Bone Marrow Stromal Cell Damage
    Baig S, Azizan AHS, Raghavendran HRB, Natarajan E, Naveen S, Murali MR, et al.
    Stem Cells Int, 2019;2019:5142518.
    PMID: 30956670 DOI: 10.1155/2019/5142518
    We have determined the protective effects of Thymus serpyllum (TS) extract and nanoparticle-loaded TS on hydrogen peroxide-induced cell death of mesenchymal stromal cells (MSCs) in vitro. Gas chromatography-mass spectroscopy confirmed the spectrum of active components in the extract. Out of the three different extracts, the hexane extract showed significant free radical scavenging activity. Treatment of MSCs with H2O2 (hydrogen peroxide) significantly increased intracellular cell death; however, pretreatment with TS extract and nanoparticle-loaded TS (200 μg/ml) suppressed H2O2-induced elevation of Cyt-c and MMP13 and increased the survival rates of MSCs. H2O2-induced (0.1 mM) changes in cytokines were attenuated in the extract and nanoparticles by pretreatment and cotreatment at two time points (p < 0.05). H2O2 increased cell apoptosis. In contrast, treatment with nanoparticle-loaded TS suppressed the percentage of apoptosis considerably (p < 0.05). Therefore, TS may be considered as a potential candidate for enhancing the effectiveness of MSC transplantation in cell therapy.
    Matched MeSH terms: Cell Death
  15. Gene expression changes in human bronchial epithelial cells (BEAS-2B) and human pulmonary alveolar epithelial cells (HPAEpiC) after interaction with Cladosporium sphaerospermum
    Lo SG, Wong SF, Mak JW, Choo KK, Ng KP
    Med Mycol, 2020 Apr 01;58(3):333-340.
    PMID: 31309220 DOI: 10.1093/mmy/myz061
    Cladosporium is one of the most abundant spore. Fungi of this genus can cause respiratory allergy and intrabronchial lesion. We studied the differential expression of host genes after the interaction of Cladosporium sphaerospermum conidia with Human Bronchial Epithelial Cells (BEAS-2B) and Human Pulmonary Alveolar Epithelial Cells (HPAEpiC). C. sphaerospermum conidia were harvested and co-cultured with BEAS-2B cells or HPAEpiC cells for 48 hours respectively. This culture duration was chosen as it was associated with high germination rate. RNA was extracted from two biological replicates per treatment. RNA of BEAS-2B cells was used to assess changes in gene expression using AffymetrixGeneChip® Human Transcriptome Array 2.0. After co-culture with Cladosporium spores, 68 individual genes were found differentially expressed (P ≤ 0.05) and up-regulated ≥ 1.5 folds while 75 genes were found differentially expressed at ≤ -1.5 folds compared with controls. Reverse transcription and qPCR were performed on the RNA collected from both BEAS-2B cells and HPAEpiC cells to validate the microarray results with 7 genes. Based on the findings, infected pulmonary epithelial cells exhibited an increase in cell death-related genes and genes associated with innate immunity.
    Matched MeSH terms: Cell Death
  16. Fulltext Neuronal Cell Death and Mouse (Mus musculus) Behaviour Induced by Bee Venom
    Oktiansyah R, Juliandi B, Widayati KA, Juniantito V
    Trop Life Sci Res, 2018 Jul;29(2):1-11.
    PMID: 30112137 DOI: 10.21315/tlsr2018.29.2.1
    Neuronal cell death can occur in a tissue or organ, including the brain, which affects memory. The objectives of this study were to determine the dose of bee venom that causes neuronal death and analyse the alteration of mouse behaviour, focusing in particular on spatial memory. Fifteen male mice of Deutsche Denken Yoken (DDY) strain were divided into control and treatment groups. Bee venom was injected six times for two weeks intraperitoneally with 1.88 mg/kg, 3.76 mg/kg, 5.6 mg/kg, and 7.48 mg/kg doses of venom. Brain histology was studied using haematoxylin-eosin stained paraffin embedded 5 μm coronal sections. A Y maze test was used to assay behaviour. Parameters observed were the number of dead neurons and the percentage of mice with altered behaviour. ANOVA showed that the effects of bee venom were significantly different in the case of the neuronal death parameter but were not significantly different in the case of the mice behaviour parameter. Duncan's Multiple Range Test (DMRT) demonstrated that P4 (7.48 mg/kg) gave the highest effect of bee venom to promote neuronal death.
    Matched MeSH terms: Cell Death
  17. Fulltext Curcumin from turmeric (Curcuma longa) induced apoptosis in human mammary carcinoma cells (MDA-MB-231)
    Latifah, S. Y., Faujan, H. A., Sze, L. P., Raha, A. R., Hisyam, A. H., Li, O. C.
    Malaysian Journal of Medicine and Health Sciences, 2006;2(2):71-79.
    MyJurnal
    Introduction: Curcumin, a natural compound present in turmeric (Curcuma longa) has been known to possess both anti-inflammatory and antioxidant effects. Objectives: The objectives of the study were to evaluate the cytotoxic activities and to determine the mode of cell death induced by curcumin towards the human mammary carcinoma cells (MDAMB-231). Methodology: Cytotoxicity of curcumin and its effect on cell viability were determined by using MTT assay and trypan blue dye exclusion method, respectively. The mode of cell death was detected by viewing under a light microscope and through DNA fragmentation analysis. Results and discussion: Curcumin was cytotoxic to MDA-MB-231 cells with the IC50 of 17.25 ì g/ml. Cell viability treatment using curcumin at concentrations of 30 ì g/ml and 10 ì g/ml was significantly (p
    Matched MeSH terms: Cell Death
  18. Fulltext Activin a: its role and involvement in inflammatory diseases
    Tie, Tung Hing, Rusliza Basir, Chuah, Yaw Kuang, Herni Talib, Norshariza Nordin
    Pertanika Journal of Science & Technology, 2015;23(2):163-176.
    MyJurnal
    Activin proteins are members of the transforming growth factor-β family. Activin A is involved in several biological responses including wound repair, cell death, proliferation and differentiation of many cell types. Biologically active activins consist of homodimers or heterodimers of two beta (β) subunits that are linked together by a single covalent disulphide bond. The subunits in humans are βA, βB, βC and βE. As an example, a combination of two βA subunits will produce a unit of activin A. These proteins are found in most cells of body such as macrophage and activated circulating monocytes. Their role in inflammation can be categorised into two types, either pro- or anti-inflammatory agents, depending on the cell type and phase. Activin signals are kept in balance by antagonist follistatin (Fst), which is a glycoprotein expressed in tissues and encoded by the follistatin gene in humans.
    Matched MeSH terms: Cell Death
  19. Neurotoxicity and neuroprotective effects of polyimides (P1) and polyphenylenevinylene (PPV) against hydrogen peroxide (H2O2)
    Norfaezah Mazalan, Mazatulikhma Mat Zain, Nor Saliyana Jumali, Norhanim Mohalid, Zurina Shameri, Ahmad Sazali Hamzah
    Scientific Research Journal, 2011;8(2):33-47.
    MyJurnal
    Recently, research and development in the field of drug delivery systems (DDS) facilitating site-specific therapy has reached significant progression. DDS based on polymer micelles, coated micro- and nanoparticles, and various prodrug systems including water-soluble polymer have been prepared and extensively studied as novel drugs designed for cancer chemotherapy and brain delivery. Since polymers are going to be used in human, this study has the interest of testing two types of polymer, polyimides (PI) and polyphenylenevinylene (PPV) on neuronal cells. The objective of this study was to determine the possible neurotoxicity and potential neuroprotective effects of PI and PPV towards SH-SY5Y neuronal cells challenged by hydrogen peroxide (1120) as an oxidant. Cells were pretreated with either PI or PPV for 1 hour followed by incubation for 24 hour with 100 ,uM of 11201. MTS • assay was used to assess cell viability. Results show that PI and PPV are not harmful within the concentration up to 10 pM and 100 pM, respectively. However, PI and PPV do not protect neuronal cells against toxicity induced by H2O, or further up the cell death.
    Matched MeSH terms: Cell Death
  20. Enterovirus A71 and coxsackievirus A16 show different replication kinetics in human neuronal and non-neuronal cell lines
    Yogarajah T, Ong KC, Perera D, Wong KT
    Arch Virol, 2017 Mar;162(3):727-737.
    PMID: 27878462 DOI: 10.1007/s00705-016-3157-4
    Enterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16) are closely related enteroviruses that cause hand, foot and mouth disease (HFMD) in children. Serious neurological complications almost always occur in EV-A71 infection, but are rare in CV-A16 infection. Based on the hypothesis that this may be because EV-A71 infects neuronal cells more easily than CV-A16, we compared virus infection, replication and spread of EV-A71 and CV-A16 in SK-N-SH cells. We found that CV-A16 invariably showed significantly lower replication and caused less necrotic cell death in SK-N-SH cells, compared with EV-A71. This was not due to a lower proportion of CV-A16-infected cells, since both viruses showed similar proportions of infected cells at all time points analyzed. Furthermore, reduced replication of CV-A16 in SK-N-SH cells does not appear to be due to limited viral receptor availability, which might limit viral entry, because experiments with viral RNA-transfected cells showed the same results as for live virus infections. On the other hand, no differences were observed between EV-A71 and CV-A16 in RD cells and results were generally similar in RD cells for both viruses. Taken together, our findings suggest that the poor growth of CV-A16 and EV-A71in SK-N-SH cells, compared with RD cells, may be due to cell type-specific restrictions on viral replication and spread. Furthermore, the lower viral replication and necrotic cell death in CV-A16-infected SK-N-SH cells, compared with EV-A71-infected SK-N-SH cells, is consistent with the lower prevalence of neurotropism observed in CV-A16-associated HFMD outbreaks. Nonetheless, in vivo data and more extensive comparisons of different viral strains are essential to confirm our findings.
    Matched MeSH terms: Cell Death
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