Displaying publications 21 - 40 of 258 in total

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  1. Biocompatibility of bio based calcium carbonate nanocrystals aragonite polymorph on NIH 3T3 fibroblast cell line
    Kamba AS, Ismail M, Ibrahim TA, Zakaria ZA
    Afr J Tradit Complement Altern Med, 2014;11(4):31-8.
    PMID: 25392577
    BACKGROUND: Currently, there has been extensive research interest for inorganic nanocrystals such as calcium phosphate, iron oxide, silicone, carbon nanotube and layered double hydroxide as a drug delivery system especially in cancer therapy. However, toxicological screening of such particles is paramount importance before use as delivery carrier. In this study we examine the biocompatibility of CaCO3 nanocrystal on NIH 3T3 cell line.

    MATERIAL AND METHODS: Transmission and field emission scanning electron microscopy (TEM and FESEM) were used for the characterisation of CaCO3 nanocrystals. Cytotoxicity and genotoxic effect of calcium carbonate nanocrystals in cultured mouse embryonic fibroblast NIH 3T3 cell line using various bioassays including MTT, and Neutral red/Trypan blue double-staining assays. LDH, BrdU and reactive oxygen species were used for toxicity analysis. Cellular morphology was examined by scanning electron microscopy (SEM) and confocal fluorescence microscope.

    RESULTS: The outcome of the analyses revealed a clear rod-shaped aragonite polymorph of calcium carbonate nanocrystal. The analysed cytotoxic and genotoxicity of CaCO3 nanocrystal on NIH 3T3 cells using different bioassays revealed no significance differences as compared to control. A slight decrease in cell viability was noticed when the cells were exposed to higher concentrations of 200 to 400 µg/ml, while increase in ROS generation and LDH released at 200 and 400 µg/ml was observed.

    CONCLUSIONS: The study has shown that CaCO3 nanocrystal is biocompatible and non toxic to NIH 3T3 fibroblast cells. The analysed results offer a promising potential of CaCO3 nanocrystal for the development of intracellular drugs, genes and other macromolecule delivery systems.

    Matched MeSH terms: Reactive Oxygen Species/metabolism
  2. Fulltext Vitamin E in sarcopenia: current evidences on its role in prevention and treatment
    Khor SC, Abdul Karim N, Ngah WZ, Yusof YA, Makpol S
    Oxid Med Cell Longev, 2014;2014:914853.
    PMID: 25097722 DOI: 10.1155/2014/914853
    Sarcopenia is a geriatric syndrome that is characterized by gradual loss of muscle mass and strength with increasing age. Although the underlying mechanism is still unknown, the contribution of increased oxidative stress in advanced age has been recognized as one of the risk factors of sarcopenia. Thus, eliminating reactive oxygen species (ROS) can be a strategy to combat sarcopenia. In this review, we discuss the potential role of vitamin E in the prevention and treatment of sarcopenia. Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways. Previous studies have shown its possible beneficial effects on aging and age-related diseases. Although there are evidences suggesting an association between vitamin E and muscle health, they are still inconclusive compared to other more extensively studied chronic diseases such as neurodegenerative diseases and cardiovascular diseases. Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and current in vitro and in vivo studies.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  3. Fulltext Phytoagents for cancer management: regulation of nucleic acid oxidation, ROS, and related mechanisms
    Lee WL, Huang JY, Shyur LF
    Oxid Med Cell Longev, 2013;2013:925804.
    PMID: 24454991 DOI: 10.1155/2013/925804
    Accumulation of oxidized nucleic acids causes genomic instability leading to senescence, apoptosis, and tumorigenesis. Phytoagents are known to reduce the risk of cancer development; whether such effects are through regulating the extent of nucleic acid oxidation remains unclear. Here, we outlined the role of reactive oxygen species in nucleic acid oxidation as a driving force in cancer progression. The consequential relationship between genome instability and cancer progression highlights the importance of modulation of cellular redox level in cancer management. Current epidemiological and experimental evidence demonstrate the effects and modes of action of phytoagents in nucleic acid oxidation and provide rationales for the use of phytoagents as chemopreventive or therapeutic agents. Vitamins and various phytoagents antagonize carcinogen-triggered oxidative stress by scavenging free radicals and/or activating endogenous defence systems such as Nrf2-regulated antioxidant genes or pathways. Moreover, metal ion chelation by phytoagents helps to attenuate oxidative DNA damage caused by transition metal ions. Besides, the prooxidant effects of some phytoagents pose selective cytotoxicity on cancer cells and shed light on a new strategy of cancer therapy. The "double-edged sword" role of phytoagents as redox regulators in nucleic acid oxidation and their possible roles in cancer prevention or therapy are discussed in this review.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  4. Neuroprotective properties of Loranthus parasiticus aqueous fraction against oxidative stress-induced damage in NG108-15 cells
    Wong DZ, Kadir HA, Lee CL, Goh BH
    J Nat Med, 2012 Jul;66(3):544-51.
    PMID: 22318341 DOI: 10.1007/s11418-011-0622-y
    Loranthus parasiticus, a Chinese folk medicine, has been widely used for the treatment of brain diseases, particularly in southwest China. Hence, the present neuroprotection model was designed to investigate its neuroprotective properties against H(2)O(2)-induced oxidative stress in NG108-15 cells. L. parasiticus aqueous fraction (LPAF), which was selected in the present study, had proved to be the most active fraction among the other tested extracts and fractions in our previous screening. The restoration of depleted intracellular glutathione (GSH), a major endogenous antioxidant, by LPAF was observed after H(2)O(2) insult. Pretreatment with LPAF substantially reduced the production of intracellular reactive oxygen species generated from H(2)O(2). Apoptotic features such as externalization of phosphatidylserine and disruption of mitochondrial membrane potential were significantly attenuated by LPAF. In addition, cell cycle analysis revealed a prominent decrease in the H(2)O(2)-induced sub-G(1) population by LPAF. Moreover, apoptotic morphological analysis by DAPI nuclear staining demonstrated that NG108-15 cells treated with H(2)O(2) exhibited apoptotic features, while such changes were greatly reduced in cells pretreated with LPAF. Taken together, these findings confirmed that LPAF exerts marked neuroprotective activity, which raises the possibility of potential therapeutic application of LPAF for managing oxidative stress-related neurological disorders and supports the traditional use of L. parasiticus in treating brain-related diseases.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  5. Fulltext Sphingosine 1-phosphate receptor 2 (S1P2) attenuates reactive oxygen species formation and inhibits cell death: implications for otoprotective therapy
    Herr DR, Reolo MJ, Peh YX, Wang W, Lee CW, Rivera R, et al.
    Sci Rep, 2016 Apr 15;6:24541.
    PMID: 27080739 DOI: 10.1038/srep24541
    Ototoxic drugs, such as platinum-based chemotherapeutics, often lead to permanent hearing loss through apoptosis of neuroepithelial hair cells and afferent neurons of the cochlea. There is no approved therapy for preventing or reversing this process. Our previous studies identified a G protein-coupled receptor (GPCR), S1P2, as a potential mediator of otoprotection. We therefore sought to identify a pharmacological approach to prevent cochlear degeneration via activation of S1P2. The cochleae of S1pr2(-/-) knockout mice were evaluated for accumulation of reactive oxygen species (ROS) with a nitro blue tetrazolium (NBT) assay. This showed that loss of S1P2 results in accumulation of ROS that precedes progressive cochlear degeneration as previously reported. These findings were supported by in vitro cell-based assays to evaluate cell viability, induction of apoptosis, and accumulation of ROS following activation of S1P2 in the presence of cisplatin. We show for the first time, that activation of S1P2 with a selective receptor agonist increases cell viability and reduces cisplatin-mediated cell death by reducing ROS. Cumulatively, these results suggest that S1P2 may serve as a therapeutic target for attenuating cisplatin-mediated ototoxicity.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  6. Antioxidant modulation in restoring mitochondrial function in neurodegeneration
    Pahrudin Arrozi A, Wan Ngah WZ, Mohd Yusof YA, Ahmad Damanhuri MH, Makpol S
    Int J Neurosci, 2017 Mar;127(3):218-235.
    PMID: 27074540 DOI: 10.1080/00207454.2016.1178261
    Alzheimer's disease (AD) and Parkinson's disease (PD) are the leading causes of disability associated with neurodegeneration worldwide. These diseases are influenced by multiple genetic and environmental factors and share similar mechanisms as both are characterized by accumulation and aggregation of misfolded proteins - amyloid-beta (Aβ) in AD and α-synuclein in PD. Over the past decade, increasing evidence has shown that mitochondrial dysfunction and the generation of reactive oxygen species (ROS) are involved in the pathology of these diseases, and the contributions of these defects to the cellular and molecular changes that eventually cause neuronal death have been explored. Using mitochondrial protective agents, such as antioxidants, to combat ROS provides a new strategy for neurodegenerative treatment. In this review, we highlight the potential of multiple types of antioxidants, including vitamins, phytochemicals, fatty acids and minerals, as well as synthetic antioxidants specifically targeting the mitochondria, which can restore mitochondrial function, in the treatment of neurodegenerative disorders at both the pre-clinical and clinical stages by focusing on AD and PD.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  7. Atherosclerotic cardiovascular disease: a review of initiators and protective factors
    Ellulu MS, Patimah I, Khaza'ai H, Rahmat A, Abed Y, Ali F
    Inflammopharmacology, 2016 Feb;24(1):1-10.
    PMID: 26750181 DOI: 10.1007/s10787-015-0255-y
    Atherosclerotic cardiovascular disease (CVD) is a collective term comprising of a group of disorders of the heart and blood vessels. These diseases are the largest cause of morbidity and premature death worldwide. Coronary heart disease and cerebrovascular disease (stroke) are the most frequently occurring diseases. The two major initiators involved in the development of atherosclerotic CVD are vascular production of reactive oxygen species (ROS) and lipid oxidation. In atherosclerosis development, ROS is associated with rapid loss of anti-inflammatory and anti-atherogenic activities of the endothelium-derived nitric oxide (NO(·)) resulting in endothelial dysfunction. In part involving activation of the transcription factor NF-κB, ROS have been involved in signaling cascades leading to vascular pro-inflammatory and pro-thrombotic gene expression. ROS is also a potent activator of matrix metalloproteinases (MMPs), which indicate plaque destabilization and rupture. The second initiator involved in atherosclerotic CVD is the oxidation of low-density lipoproteins (LDL). Oxidation of LDL in vessel wall leads to an inflammatory cascade that activates atherogenic pathway leading to foam cell formation. The accumulation of foam cells leads to fatty streak formation, which is the earliest visible atherosclerotic lesion. In contrast, the cardiac sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA2a) and hepatic apolipoprotein E (apoE) expression can improve cardiovascular function. SERCA2a regulates the cardiac contractile function by lowering cytoplasmic calcium levels during relaxation, and affecting NO(·) action in vascular cells, while apoE is a critical ligand in the plasma clearance of triglyceride- and cholesterol-rich lipoproteins.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  8. Fulltext Major pathophysiological correlations of rosacea: a complete clinical appraisal
    Vemuri RC, Gundamaraju R, Sekaran SD, Manikam R
    Int J Med Sci, 2015;12(5):387-96.
    PMID: 26005373 DOI: 10.7150/ijms.10608
    Rosacea is a characteristic cutaneous disorder with a diverse clinical manifestations ranging from facial vascular hyper-reactivity to sebaceous gland hyperplasia. Many theories on pathophysiology of rosacea were proposed over the past decade, however the pathogenicity is poorly understood.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  9. Fulltext Impact of elevated temperature on the physiological and biochemical responses of Kappaphycus alvarezii (Rhodophyta)
    Kumar YN, Poong SW, Gachon C, Brodie J, Sade A, Lim PE
    PLoS One, 2020;15(9):e0239097.
    PMID: 32925956 DOI: 10.1371/journal.pone.0239097
    The eucheumatoids Kappaphycus and Eucheuma are cultivated in tropical or subtropical regions for the production of carrageenan, a hydrocolloid widely used in the food and cosmetic industries. Kappaphycus alvarezii is a highly valued economic crop in the Coral Triangle, with the Philippines, Indonesia and Malaysia ranked among the largest producers. In the absence of measures to mitigate climate change, extreme events including heatwaves, typhoons, severe El Niño and La Niña, are expected to increase in frequency and magnitude. This inadvertently brings adverse effects to the seaweed cultivation industry, especially in the tropics. Temperatures are rapidly reaching the upper limit of biologically tolerable levels and an increase in reports of ice-ice and pest outbreaks is attributable to these shifts of environmental parameters. Nevertheless, few reports on the response of eucheumatoids to a changing environment, in particular global warming, are available. Understanding the responses and possible mechanisms for acclimation to warming is crucial for a sustainable seaweed cultivation industry. Here, the physiological and biochemical responses of K. alvarezii to acute warming indicated that the strain used in the current study is unlikely to survive sudden increases in temperature above 36°C. As temperature increased, the growth rates, photosynthetic performance, phycocolloid quality (carrageenan yield, gel strength and gel viscosity) and pigment content (chlorophyll-a, carotenoid and phycobiliproteins) were reduced while the production of reactive oxygen species increased indicating the occurrence of stress in the seaweeds. This study provides a basis for future work on long term acclimation to elevated temperature and mesocosm-based multivariate studies to identify heat-tolerant strains for sustainable cultivation.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  10. Mitochondrial dysfunction as a central event for mechanisms underlying insulin resistance: the roles of long chain fatty acids
    Hafizi Abu Bakar M, Kian Kai C, Wan Hassan WN, Sarmidi MR, Yaakob H, Zaman Huri H
    Diabetes Metab Res Rev, 2015 Jul;31(5):453-75.
    PMID: 25139820 DOI: 10.1002/dmrr.2601
    Insulin resistance is characterized by hyperglycaemia, dyslipidaemia and oxidative stress prior to the development of type 2 diabetes mellitus. To date, a number of mechanisms have been proposed to link these syndromes together, but it remains unclear what the unifying condition that triggered these events in the progression of this metabolic disease. There have been a steady accumulation of data in numerous experimental studies showing the strong correlations between mitochondrial dysfunction, oxidative stress and insulin resistance. In addition, a growing number of studies suggest that the raised plasma free fatty acid level induced insulin resistance with the significant alteration of oxidative metabolism in various target tissues such as skeletal muscle, liver and adipose tissue. In this review, we herein propose the idea of long chain fatty acid-induced mitochondrial dysfunctions as one of the key events in the pathophysiological development of insulin resistance and type 2 diabetes. The accumulation of reactive oxygen species, lipotoxicity, inflammation-induced endoplasmic reticulum stress and alterations of mitochondrial gene subset expressions are the most detrimental that lead to the developments of aberrant intracellular insulin signalling activity in a number of peripheral tissues, thereby leading to insulin resistance and type 2 diabetes.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  11. 4-chloro-1,2-phenylenediamine induces apoptosis in Mardin-Darby canine kidney cells via activation of caspases
    Onn LC, Ching CS, Lian TY, Foon LV, Chew Hee N, Moi CS
    Environ Toxicol, 2014 Jun;29(6):655-64.
    PMID: 22778066 DOI: 10.1002/tox.21792
    4-Chloro-1,2-phenylenediamine (4-Cl-o-PD) is a halogenated aromatic diamine that was used as a precursor for manufacturing permanent hair dyes. Despite its well-documented mutagenic and carcinogenic effects in a number of in vitro and in vivo models, its cytotoxicity and mode of action have not received similar attention. Here, we investigated the effect of 4-Cl-o-PD on Mardin-Darby canine kidney cells. It induced apoptosis and the evidence suggests its initiation by reactive oxygen species (ROS). The results of various assays used show a dose-dependent (i) decrease in cell viability, (ii) increase in cells at sub-G1 phase and the G0/G1 phase arrested in cell cycle, (iii) increase in intracellular ROS accompanied by depletion of glutathione, and (iv) that apoptotic cell death probably involves activation of both intrinsic and extrinsic pathways.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  12. Vernodalin induces apoptosis through the activation of ROS/JNK pathway in human colon cancer cells
    Mohebali N, Pandurangan AK, Mustafa MR, Anandasadagopan SK, Alagumuthu T
    J Biochem Mol Toxicol, 2020 Dec;34(12):e22587.
    PMID: 32726518 DOI: 10.1002/jbt.22587
    Colorectal cancer is one of the most leading death-causing cancers in the world. Vernodalin, a cytotoxic sesquiterpene, has been reported to possess anticancer properties against human breast cancer cells. We aimed to examine the anticancer mechanism of vernodalin on human colon cancer cells. Vernodalin was used on human colon cancer cells, HT-29 and HCT116. The cytotoxicity of vernodalin on human colon cancer cells was determined through in vitro 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Small interfering RNA was used to analyze the cascade activation of mitogen-activated protein kinase (MAPK) pathway, c-Jun N-terminal kinase (JNK) in HT-29, and HCT116 cells against vernodalin treatment. The protein expressions of caspase 3, Bcl-2, and Bax were examined through Western blot analysis. Immunoblot analysis on the JNK, ERK, and p38 MAPK pathways showed increased activation due to vernodalin treatment. It was proven from the JNK and p38 inhibition test that both pathways are significantly activated by vernodalin to induce apoptosis. Our results, collectively, showed the apoptosis-induced anticancer mechanism of vernodalin on human colon cancer cells that was mediated through the activation of JNK pathway and apoptotic regulator proteins. These results suggest that vernodalin could be developed as a potent chemotherapeutic agent for human colorectal cancer treatment.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  13. Possible Anticancer Mechanisms of Some Costus speciosus Active Ingredients Concerning Drug Discovery
    El-Far AH, Badria FA, Shaheen HM
    Curr Drug Discov Technol, 2016;13(3):123-143.
    PMID: 27515456
    Costus speciosus is native to South East Asia, especially found in India, Srilanka, Indonesia and Malaysia. C. speciosus have numerous therapeutic potentials against a wide variety of complains. The therapeutic properties of C. speciosus are attributed to the presence of various ingredients such as alkaloids, flavonoids, glycosides, phenols, saponins, sterols and sesquiterpenes. This review presented the past, present, and the future status of C. speciosus active ingredients to propose a future use as a potential anticancer agent. All possible up-regulation of cellular apoptotic molecules as p53, p21, p27, caspases, reactive oxygen species (ROS) generation and others attribute to the anticancer activity of C. speciosus along the down-regulation of anti-apoptotic agents such as Akt, Bcl2, NFKB, STAT3, JAK, MMPs, actin, surviving and vimentin. Eventually, we recommend further investigation of different C. speciosus extracts, using some active ingredients and evaluate the anticancer effect of these chemicals against different cancers.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  14. Zinc and Metallothionein in the Development and Progression of Dental Caries
    Rahman MT, Hossain A, Pin CH, Yahya NA
    Biol Trace Elem Res, 2019 Jan;187(1):51-58.
    PMID: 29744817 DOI: 10.1007/s12011-018-1369-z
    Chronic oxidative stress and reactive oxygen species (ROS) in oral cavity as well as acidic pH on dental enamel surface due to the metabolic activities of bacterial plaque are the major contributors in the development and progression of dental caries. Along with other factors, deposition or dissolution Ca and Mg mostly determines the re- or demineralization of dental enamel. Zn plays an important role for both Ca and Mg bioavailability in oral cavity. Metallothionein (MT), a group of small molecular weight, cysteine-rich proteins (~ 7 kDa), is commonly induced by ROS, bacterial infection, and Zn. In the current review, we evaluated MT at the junction between the progression of dental caries and its etiologies that are common in MT biosynthesis.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  15. Metabolic Syndrome and Its Effect on the Brain: Possible Mechanism
    Arshad N', Lin TS, Yahaya MF
    CNS Neurol Disord Drug Targets, 2018;17(8):595-603.
    PMID: 30047340 DOI: 10.2174/1871527317666180724143258
    BACKGROUND & OBJECTIVE: Metabolic syndrome (MetS) is an interconnected group of physiological, biochemical, clinical and metabolic factors that directly increase the risk of cardiovascular disease, type 2 diabetes mellitus (T2DM) and mortality. Rising evidence suggests that MetS plays a significant role in the progression of Alzheimer's disease and other neurodegenerative diseases. Nonetheless, the factors linking this association has not yet been elucidated. As we are facing an increasing incidence of obesity and T2DM in all stages of life, understanding the association of MetS and neurodegenerative diseases is crucial to lessen the burden of the disease.

    CONCLUSION: In this review, we will discuss the possible mechanisms which may relate the association between MetS and cognitive decline which include vascular damages, elevation of reactive oxygen species (ROS), insulin resistance and low-grade inflammation.

    Matched MeSH terms: Reactive Oxygen Species/metabolism
  16. Modulation of age related protein expression changes by gelam honey in cardiac mitochondrial rats
    Hasenan SM, Karsani SA, Jubri Z
    Exp Gerontol, 2018 11;113:1-9.
    PMID: 30248357 DOI: 10.1016/j.exger.2018.09.001
    Aging is characterized by progressive decline in biochemical and physiological functions. According to the free radical theory of aging, aging results from oxidative damage due to the accumulation of excess reactive oxygen species (ROS). Mitochondria are the main source of ROS production and are also the main target for ROS. Therefore, a diet high in antioxidant such as honey is potentially able to protect the body from ROS and oxidative damage. Gelam honey is higher in flavonoid content and phenolic compounds compared to other local honey. This study was conducted to determine the effects of gelam honey on age related protein expression changes in cardiac mitochondrial rat. A total of 24 Sprague-Dawley male rats were divided into two groups: the young group (2 months old), and aged group (19 months old). Each group were then subdivided into two groups: control group (force-fed with distilled water), and treatment group (force-fed with gelam honey, 2.5 g/kg), and were treated for 8 months. Comparative proteomic analysis of mitochondria from cardiac tissue was then performed by high performance mass spectrometry (Q-TOF LCMS/MS) followed by validation of selected proteins by Western blotting. Proteins were identified using Spectrum Mill software and were subjected to stringent statistical analysis. A total of 286 proteins were identified in the young control group (YC) and 241 proteins were identified in the young gelam group (YG). In the aged group, a total of 243 proteins were identified in control group (OC), and 271 proteins in gelam group (OG). Comparative proteome profiling identified 69 proteins with different abundance (p 
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  17. Fulltext Cephalomannine inhibits hypoxia-induced cellular function via the suppression of APEX1/HIF-1α interaction in lung cancer
    Ullah A, Leong SW, Wang J, Wu Q, Ghauri MA, Sarwar A, et al.
    Cell Death Dis, 2021 05 14;12(5):490.
    PMID: 33990544 DOI: 10.1038/s41419-021-03771-z
    Lung cancer (LC) is one of the leading causes of cancer-related death. As one of the key features of tumor microenvironment, hypoxia conditions are associated with poor prognosis in LC patients. Upregulation of hypoxic-induced factor-1α (HIF-1α) leads to the activation of various factors that contribute to the increased drug resistance, proliferation, and migration of tumor cells. Apurinic/apyrimidinic endonuclease-1 (APEX1) is a multi-functional protein that regulates several transcription factors, including HIF-1α, that contribute to tumor growth, oxidative stress responses, and DNA damage. In this study, we explored the mechanisms underlying cell responses to hypoxia and modulation of APEX1, which regulate HIF-1α and downstream pathways. We found that hypoxia-induced APEX1/HIF-1α pathways regulate several key cellular functions, including reactive oxygen species (ROS) production, carbonic anhydrase 9 (CA9)-mediated intracellular pH, migration, and angiogenesis. Cephalomannine (CPM), a natural compound, exerted inhibitory effects in hypoxic LC cells via the inhibition of APEX1/HIF-1α interaction in vitro and in vivo. CPM can significantly inhibit cell viability, ROS production, intracellular pH, and migration in hypoxic LC cells as well as angiogenesis of HUVECs under hypoxia through the inhibition of APEX1/HIF-1α interaction. Taken together, CPM could be considered as a promising compound for LC treatment.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  18. CONJUGATION WITH SILVER NANOPARTICLES ENHANCES ANTI-ACANTHAMOEBIC ACTIVITY OF KAPPAPHYCUS ALVAREZII
    Walvekar S, Anwar A, Anwar A, Lai NJY, Yow YY, Khalid M, et al.
    J Parasitol, 2021 07 01;107(4):537-546.
    PMID: 34265050 DOI: 10.1645/21-41
    Nanomedicine has the potential in enhancing the efficacy and bioavailability of anti-infective agents. Here we determined whether conjugation of the Malaysian cultivated seaweed Kappaphycus alvarezii with silver-conjugated nanoparticles enhanced anti-acanthamoebic properties. Silver-conjugated K. alvarezii were successfully synthesized, followed by characterization with Fourier transform infrared spectroscopy, ultraviolet-visible spectrophotometry, and transmission electron microscopy. Amoebicidal effects were evaluated against Acanthamoeba castellanii, and cytotoxicity assays were performed using HaCaT cells. Viability assays revealed that silver nanoparticles conjugated with K. alvarezii extract exhibited significant antiamoebic properties (P < 0.05). Nano-conjugates induced the production of reactive oxygen species. Importantly, silver-conjugated extract inhibited amoeba-mediated host cell damage as established by lactate dehydrogenase release. Neither the nano-conjugates nor the extract showed cytotoxicity against human cells in vitro. Liquid chromatography and mass spectroscopy revealed several molecules, including 2,6-nonadien-1-ol, N-desmethyl trifluoperazine, dulciol B, lucidumol A, acetoxolone, 2-[4,6-bis(2,4-dimethylphenyl)-1,3,5-triazin-2-yl]-5-(octyloxy)phenol, C16 sphinganine, 22-tricosenoic acid, and β-dihydrorotenone, of which dulciol B and C16 sphinganine are known to possess antimicrobial activities. In summary, marine organisms are an important source of bioactive molecules with anti-acanthamoebic properties that can be enhanced by conjugating with silver nanoparticles. Natural products combined with nanotechnology using multifunctional nanoparticle complexes can deliver therapeutic agents effectively and hold promise in the development of new formulations of anti-acanthamoebic agents.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  19. S-phase arrest and apoptosis in human breast adenocarcinoma MCF-7 cells via mitochondrial dependent pathway induced by tricyclohexylphosphine gold (I) n-mercaptobenzoate complexes
    Pian AK, Foong CP, Hamid RA
    Life Sci, 2022 Dec 15;311(Pt B):121161.
    PMID: 36375571 DOI: 10.1016/j.lfs.2022.121161
    We have previously reported the inhibition of thioredoxin reductase (TrxR) and invasion by tricyclohexylphosphine gold (I) n-mercaptobenzoate (n = 2, 3, 4) labeled as 1-3 towards MCF-7 cells, in vitro. Nevertheless, the mode of death and its apoptotic pathway has yet to be revealed. The main aim of this study is to investigate the anti-neoplastic activity of this phosphanegold (I) thiolates against breast adenocarcinoma cells, MCF-7. Herein, we explored the role of gold(I) series, 1-3 for their apoptosis-inducing ability against MCF-7 cells. They were scrutinized for their antiproliferative activities which exhibited their IC50 values of 8.14 μM ± 0.10, 7.26 μM ± 0.33, and 9.03 μM ± 0.69, respectively, and indicated better cytotoxicities than that of cisplatin (positive control). Further, the mechanisms of their actions were studied by analyzing the status of ROS generation (by DCFH-DA), cytochrome c release (by ELISA), and activation of caspases 3/7, 8, 9, and 10, annexin V staining and cell cycle analysis by flow cytometry, respectively. It was observed that the compounds, 1-3 can promote ROS generation, cytochrome c release, and activation of caspases 3/7, caspase 8, caspase 9, and caspase 10 on MCF-7 cells. In addition, the compounds are shown to induce MCF-7 cell arrest at S-phase. Gene analysis via PCR array further clarified their effects by modulating the related genes upon the compounds' treatment. Further investigation on other breast cancer cells as well as in vivo studies on these compounds will further increase their potential as anti-breast cancer agents.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  20. Fulltext Kaempferol ameliorates palmitate-induced lipid accumulation in HepG2 cells through activation of the Nrf2 signaling pathway
    Zhao L, Yang L, Ahmad K
    Hum Exp Toxicol, 2023;42:9603271221146780.
    PMID: 36607234 DOI: 10.1177/09603271221146780
    OBJECTIVES: Kaempferol (KMF), has beneficial effects against hepatic lipid accumulation. In this study, we aimed to investigate molecular mechanism underlying the protective effect of KMF on lipid accumulation.

    METHODS: HepG2 cells were treated with different concentrations of KMF and 0.5 mM palmitate (PA) for 24  h. The mRNA and protein levels of genes involved in lipid metabolism were evaluated using real-time PCR and western blot. The expression of Nrf2 was silenced using siRNA.

    RESULTS: Data indicated that KMF (20 μM) reversed PA-induced increased triglyceride (TG) levels and total lipid content. These effects were accompanied by down-regulation of the mRNA and protein levels of lipogenic genes (FAS, ACC and SREBP1), and up-regulation of genes related to fatty acid oxidation (CPT-1, HADHα and PPARα). Kaempferol significantly decreased the levels of the oxidative stress markers (ROS and MDA) and enhanced the activities of antioxidant enzymes SOD and GPx in PA-challenged cells. Luciferase analysis showed that KMF increased the transactivation of Nrf2 in hepatocytes. The results also revealed that KMF-mediated activation of Nrf2 target genes was suppressed by Nrf2 siRNA. Furthermore, Nrf2 siRNA abolished the KMF-induced reduction in ROS and MDA levels in PA treated cells. In addition, the inhibitory effect of KMF on TG levels and the mRNA and protein levels of FAS, ACC and SREPB-1 were significantly abolished by Nrf2 inhibition. Nrf2 inhibition also suppressed the KMF-induced activation of genes involved in β oxidation (CPT-1 and PPAR-α).

    CONCLUSION: The results suggest that KMF protects HepG2 cells from PA-induced lipid accumulation via activation of the Nrf2 signaling pathway.

    Matched MeSH terms: Reactive Oxygen Species/metabolism
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