9 results on '"Jufri NF"'
Search Results
2. Cellular and DNA Toxicity Study of Triphenyltin Ethyl Phenyl Dithiocarbamate and Triphenyltin Butyl Phenyl Dithiocarbamate on K562, Leukemia Cell Line.
- Author
-
Hamid A, Rajab NF, Charmagne Y, Awang N, Jufri NF, and Rasli NR
- Subjects
- Humans, K562 Cells, DNA Damage, Organotin Compounds pharmacology, Antineoplastic Agents pharmacology, Leukemia drug therapy
- Abstract
Introduction: Continuous research for new effective drugs to treat cancer has improved our understanding on the mechanism of action of these drugs and paved new potential for their application in cancer treatments. In this study, organotin compounds known as triphenyltin ethyl phenyl dithiocarbamate and triphenyltin butyl phenyl dithiocarbamate were investigated for their toxicity on leukemia cell line (K562) and non-cancerous cell line (Chang liver cell and lung fibroblast, V79 cell)., Methods: MTT assay was performed to evaluate the cytotoxic effects of both compounds toward the cells after 24, 48 and 72 hours of exposure or treatment. The alkaline comet assay was conducted to determine the DNA damage on K562 cells after been exposed to both compounds for 30, 60 and 90 minutes., Results: The IC
50 values obtained from K562 cells ranged from 0.01 to 0.30 μM, whereas for both Chang liver cell and lung fibroblast V79 cell, the values ranged from 0.10 to 0.40 μM. For genotoxicity evaluation, the percentage of damaged DNA is measured as an average of tail moment, and was found to be within 1.20 to 2.20 A.U while the percentage of DNA intensity ranging from 1.50 to 3.50% indicating no genotoxic effects., Conclusion: Both compounds are cytotoxic toward leukemia cells and non-cancerous cells but do not exert their genotoxic effects towards leukemia cell., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)- Published
- 2024
- Full Text
- View/download PDF
3. Lysosomal dysfunction induced cytosolic vacuolation and increased intracellular amyloid-beta 42 (Aβ42) in human brain endothelial cells (HBEC-5i).
- Author
-
Laili IN, Nasir MHM, Jufri NF, Ibrahim FW, and Hamid A
- Subjects
- Humans, Cytosol metabolism, Amyloid beta-Peptides metabolism, Brain metabolism, Lysosomes metabolism, Disease Progression, Endothelial Cells metabolism, Alzheimer Disease metabolism
- Abstract
Lysosome is a primary degradative organelle and is crucial in cellular homeostasis. A reduction in its function due to ageing has been associated with the development of Alzheimer's disease (AD), a common neurodegenerative disorder characterised by the deposition of neurotoxic amyloid plaque in the brain and cerebral vessel walls. The breakdown of the blood-brain barrier (BBB) plays a vital role in the pathogenesis of AD. However, the impact of lysosomal dysfunction on brain endothelial cells, the key component of the BBB, in the disease progression is yet to be fully understood. In this study, human brain endothelial cells (HBEC-5i) were exposed to a lysosomotropic compound, chloroquine (CQ) for 24 h. Cell viability was assessed with the 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay to determine the inhibitory concentration (IC) at IC
10 (17.5 µM), IC25 (70.5 µM), and IC50 (125 µM). The morphological changes observed include vacuoles arrested in the cytosols and cell shrinkage that were more prominent at IC25 and IC50 . Lysosomal dysfunction was evaluated by measuring the lysosomal-associated membrane protein-1 (LAMP-1) and microtubule-associated protein light chain 3-II (LC3-II) using the capillary-based immunoassay. LC3-II was significantly increased at IC25 and IC50 (p < 0.05 and p < 0.001, respectively). The concentration of intracellular and extracellular Aβ42 was quantitated using the enzyme-linked immunosorbent assay, which demonstrated a significant increase (p < 0.05) in intracellular Aβ42 at IC25 . This study showed that perturbation of lysosomal function impairs autophagy that leads to intracellular increment of Aβ, indicating the important roles of lysosomes in endothelial cells homeostasis and disease progression., Competing Interests: Conflict of interest statement The authors declare that there are no conflicts of interest in this work., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)- Published
- 2023
- Full Text
- View/download PDF
4. Hyperphagia in Prader-Willi syndrome with obesity: From development to pharmacological treatment.
- Author
-
Rahman QFA, Jufri NF, and Hamid A
- Abstract
Prader-Willi syndrome (PWS) is a rare genetic disorder due to lack of genes expression inherited from the paternal chromosome 15q11-q13 region usually from paternal deletions, maternal uniparental disomy 15 or imprinting defect. There are two different nutritional stages reported in an individual with PWS; first stage during infancy marked by feeding and growth difficulties and second stage where hyperphagia starts and leads to development of obesity. However, the exact mechanism of hyperphagia development, from having difficulties in feeding during early years to insatiable appetite after they grow is still unknown and is the focused in this review. The keywords used for literature search such as "Prader-Willi syndrome", "hyperphagia", "obesity", and "treatment" were used to create the search strings by using synonyms in order to retrieve the relevant records from PubMed, Scopus and Science Direct. The possible mechanism of hyperphagia can be classed into hormonal abnormalities such as increase in ghrelin and leptin from infancy to adulthood. Low level of hormones was observed in the thyroid, insulin and peptide YY at certain ages. Neuronal abnormalities contributed by Orexin A and brain structure alteration was documented at 4-30 years old. Treatment in the form of drugs such as livoletide, topiramate, and diazoxide could potentially alleviate these abnormalities and make hyperphagia less prominent in PWS. The approaches are important to regulate the hormonal changes and neuronal involvement as potentially controlling hyperphagia and obesity., Competing Interests: The authors have no conflicts of interest to disclose., (2023, International Research and Cooperation Association for Bio & Socio - Sciences Advancement.)
- Published
- 2023
- Full Text
- View/download PDF
5. Classical and alternative receptors for SARS-CoV-2 therapeutic strategy.
- Author
-
Masre SF, Jufri NF, Ibrahim FW, and Abdul Raub SH
- Subjects
- Angiotensin-Converting Enzyme 2 genetics, Angiotensin-Converting Enzyme 2 metabolism, Animals, COVID-19 genetics, COVID-19 virology, Humans, Receptors, Virus genetics, SARS-CoV-2 genetics, Virus Internalization, COVID-19 Drug Treatment, COVID-19 metabolism, Receptors, Virus metabolism, SARS-CoV-2 physiology
- Abstract
Understanding the molecules that are essential for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) entry can provide insights into viral infection and dissemination. Recently, it has been identified from several studies that angiotensin-converting enzyme 2 receptor and transmembrane serine protease 2 are the main entry molecules for the SARS-CoV-2, which produced the pandemic of Covid-19. However, additional evidence showed several other viral receptors and cellular proteases that are also important in facilitating viral entry and transmission in the target cells. In this review, we summarized the types of SARS-CoV-2 entry molecules and discussed their crucial roles for virus binding, protein priming and fusion to the cellular membrane important for SARS-CoV-2 infection., (© 2020 John Wiley & Sons Ltd.)
- Published
- 2021
- Full Text
- View/download PDF
6. Hepatoprotective Effects of Zerumbone against Paracetamol-Induced Acute Hepatotoxicity in Rats.
- Author
-
Hamid A, Lee LS, Karim SR, and Jufri NF
- Abstract
Background: Zerumbone (ZER) is a major bioactive compound of Zingiber zerumbet, a wild ginger plant that has been documented to have anti-proliferative, anti-inflammatory and anti-oxidant properties. To investigate its hepatoprotective potential, this study was designed to determine the treatment effects of ZER on acute hepatotoxicity induced by paracetamol (PCM) in rats., Methods: The control group was administered with phosphate buffer solution (PBS) while the other two groups received PCM alone (1000 mg/kg) and PCM + 25 mg/kg ZER, respectively, at 0 h and 4 h after PCM injection. After 24 h, the blood and liver were collected for differential white blood cell count, liver histological observation and biochemical analysis including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total protein concentration in serum and liver., Results: Treatment with ZER was found to significantly reduce ALT ( P = 0.041), AST ( P = 0.044) and total hepatic protein ( P = 0.045) in comparison to PCM-induced rats. Rats treated with ZER exhibited the normal structure of hepatocytes with no vacuolisation or necrosis and showed significantly reduced neutrophil count ( P = 0.037). This finding suggests its ability to suppress the inflammatory processes caused by PCM overdosage and decrease the hepatocytes tendency to go through necrotic processes., Conclusion: ZER possessed protective activity against PCM-induced acute hepatotoxicity in a rat model., Competing Interests: Conflict of Interest The authors declare that they have no competing interests.
- Published
- 2018
- Full Text
- View/download PDF
7. Pulsatile stretch as a novel modulator of amyloid precursor protein processing and associated inflammatory markers in human cerebral endothelial cells.
- Author
-
Gangoda SVS, Avadhanam B, Jufri NF, Sohn EH, Butlin M, Gupta V, Chung R, and Avolio AP
- Subjects
- Amyloid Precursor Protein Secretases analysis, Aspartic Acid Endopeptidases analysis, Cells, Cultured, Gene Expression Profiling, Humans, Intercellular Adhesion Molecule-1 analysis, Models, Biological, Nitric Oxide Synthase Type III analysis, Stress, Mechanical, Alzheimer Disease pathology, Amyloid beta-Protein Precursor analysis, Cytological Techniques methods, Endothelial Cells pathology, Pulse
- Abstract
Amyloid β (Aβ) deposition is a hallmark of Alzheimer's disease (AD). Vascular modifications, including altered brain endothelial cell function and structural viability of the blood-brain barrier due to vascular pulsatility, are implicated in AD pathology. Pulsatility of phenomena in the cerebral vasculature are often not considered in in vitro models of the blood-brain barrier. We demonstrate, for the first time, that pulsatile stretch of brain vascular endothelial cells modulates amyloid precursor protein (APP) expression and the APP processing enzyme, β-secretase 1, eventuating increased-Aβ generation and secretion. Concurrent modulation of intercellular adhesion molecule 1 and endothelial nitric oxide synthase (eNOS) signaling (expression and phosphorylation of eNOS) in response to pulsatile stretch indicates parallel activation of endothelial inflammatory pathways. These findings mechanistically support vascular pulsatility contributing towards cerebral Aβ levels.
- Published
- 2018
- Full Text
- View/download PDF
8. Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.
- Author
-
Jufri NF, Mohamedali A, Avolio A, and Baker MS
- Abstract
Vascular endothelial cells are subjected to hemodynamic forces such as mechanical stretch due to the pulsatile nature of blood flow. Mechanical stretch of different intensities is detected by mechanoreceptors on the cell surface which enables the conversion of external mechanical stimuli to biochemical signals in the cell, activating downstream signaling pathways. This activation may vary depending on whether the cell is exposed to physiological or pathological stretch intensities. Substantial stretch associated with normal physiological functioning is important in maintaining vascular homeostasis as it is involved in the regulation of cell structure, vascular angiogenesis, proliferation and control of vascular tone. However, the elevated pressure that occurs with hypertension exposes cells to excessive mechanical load, and this may lead to pathological consequences through the formation of reactive oxygen species, inflammation and/or apoptosis. These processes are activated by downstream signaling through various pathways that determine the fate of cells. Identification of the proteins involved in these processes may help elucidate novel mechanisms involved in vascular disease associated with pathological mechanical stretch and could provide new insight into therapeutic strategies aimed at countering the mechanisms' negative effects.
- Published
- 2015
- Full Text
- View/download PDF
9. Estrogen signaling through estrogen receptor beta and G-protein-coupled estrogen receptor 1 in human cerebral vascular endothelial cells: implications for cerebral aneurysms.
- Author
-
Tu J and Jufri NF
- Subjects
- Cell Line, Cell Membrane metabolism, Cell Nucleus metabolism, Cerebellum metabolism, Cerebellum pathology, Endothelial Cells metabolism, Estradiol pharmacology, Female, Humans, Intracranial Aneurysm metabolism, Intracranial Aneurysm pathology, Signal Transduction, Estrogen Receptor beta genetics, Estrogens genetics, Intracranial Aneurysm genetics, Receptors, Estrogen genetics, Receptors, G-Protein-Coupled genetics
- Abstract
Little is known about estrogen receptors and their signaling mechanisms in human cerebral vascular endothelial cells, which is important for understanding cerebral aneurysm pathogenesis in menopausal and postmenopausal women. Estrogen receptor beta (ERβ) and G-protein-coupled receptor 1 (GPER1) were immunocytochemically identified in human cerebral vascular endothelial cells (HCVECs). ERβ was mainly located at the nuclei of the cells while GPER1 was located at the plasma membrane. Interaction events between 17β-estradiol and ERβ or GPER1 in HCVECs were evaluated by in situ proximity ligation assay. The number of interaction events between 17β-estradiol and ERβ was positively correlated with 17β-estradiol concentrations (r = 0.9614, P < 0.01). The interaction events between 17β-estradiol and GPER1 were dose responsive. Our data support HCVECs to serve as a suitable cellular model for studying cerebral aneurysm pathogenesis in menopausal and postmenopausal women. Subtypes of estrogen receptors and their signaling mechanisms identified in HCVECs could be applicable for developing estrogen-like compounds to specifically bind to a subtype of estrogen receptors with greater specific action on the cerebral arteries, without the estrogen-dependent side effects on the reproductive organs, to prevent cerebral aneurysm formation in menopausal and postmenopausal woman.
- Published
- 2013
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.