School Of Basic And Applied Sciences

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    Role of curcumin on monoamine oxidase(MAO) enzyme expression and activity against Amyloid Beta (A?)-induced oxidative stress in human glioblastoma U-87 MG cell.
    (Central University of Punjab, 2018) Behera, Nishibala N; Mantha,Anil K.
    Glioblastoma (GBM) is the most common brain tumor in humans. The major factor responsible for its progression is oxidative stress. Oxidative stress leads to disruption of signaling pathways and damage to cells and tissues. Monoamine oxidase (MAO) is involved in oxidative deamination of endogenous biogenic amine neurotransmitters such as dopamine, serotonin, norepinephrine, and epinephrine. Therefore, MAO plays a key role in initiation and progression of GBM through oxidative stress. In the present study, A?(25-35) peptide treatment was used to induce oxidative stress in human glioblastoma (U-87 MG) cells. A?(25-35) is known to induce oxidative stress through altering the expression and activity of various antioxidant and mitochondrial enzymes. In this study, the expression and activity of MAO was evaluated through induction of oxidative stress by A?(25-35) and antioxidant treatment of Curcumin. It was found that Curcumin decreases the mRNA expression of MAO but its protein expression increases, whereas A?(25-35) showed little decrease in the mRNA expression of MAO and increase in its protein expression, thus pointing towards differential regulation of translation and transcription. The activity of MAO was found to be increased in A?(25-35), Cur and Cur+A?(25-35) . Therefore, Curcumin has little or no antioxidant effect in altering the expression and activity of MAO and A? showed its oxidative potential by increasing the expression and activity of MAO, although not very significant, possibly because it uses other pathways for inducing oxidative stress.
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    Evaluating anti-oxidant potential of ganoderic acid A in STAT 3 pathway in prostate cancer
    (Springer Netherlands, 2016) Gill, Balraj Singh; Kumar, Sanjeev; Navgeet
    Evaluating anti-oxidant potential of Ganoderic acid A in STAT 3 pathway in Prostate cancer. Molecular docking and ADMET activities of different isoforms of ganoderic acid on STAT 3 pathway were performed by Maestro 9.6 (Schr�dinger Inc). The ganoderic acid A is best-docked among isoforms which analyses the expression level of antioxidant and STAT 3 pathway in PC-3 cells. The receptor-based molecular docking reveals the best binding interaction of SH2 domain of STAT3 and ganoderic acid A with GScore (?6.134), kcal/mol, Lipophilic EvdW (?1.83), Electro (?1.1), Glide emodel (?31.857), H bond (1.98), MM-GBSA (?69.555). The molecular docking QikProp analyzed the absorption, distribution, metabolism, excretion, and toxicity (ADME/T). The ganoderic acid A is best-docked among isoforms which downregulates the expression of STAT 3 in PC-3 cells. Moreover, ganoderic acid A inhibits proliferation, viability, ROS, DPPH, and analyzed the expression of SOD1, SOD2, and SOD3 by Real time PCR in a PC-3 cell in a dose-dependent manner. Molecular docking revealed the mechanistic binding of Ganoderic acid A in STAT3 signaling, which inhibits the proliferation, viability, and ROS in PC-3 cells. � 2016, Springer Science+Business Media Dordrecht.
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    APE1/Ref-1 as an emerging therapeutic target for various human diseases: Phytochemical modulation of its functions
    (Nature Publishing Group, 2014) Thakur, Shweta; Sarkar, Bibekananda; Cholia, Ravi P.; Gautam, Nandini; Dhiman, Monisha; Mantha, Anil K.
    Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme involved in the base excision repair (BER) pathway, which repairs oxidative base damage caused by endogenous and exogenous agents. APE1 acts as a reductive activator of many transcription factors (TFs) and has also been named redox effector factor 1, Ref-1. For example, APE1 activates activator protein-1, nuclear factor kappa B, hypoxia-inducible factor 1a, paired box gene 8, signal transducer activator of transcription 3 and p53, which are involved in apoptosis, inflammation, angiogenesis and survival pathways. APE1/Ref-1 maintains cellular homeostasis (redox) via the activation of TFs that regulate various physiological processes and that crosstalk with redox balancing agents (for example, thioredoxin, catalase and superoxide dismutase) by controlling levels of reactive oxygen and nitrogen species. The efficiency of APE1/Ref-1's function(s) depends on pairwise interaction with participant protein(s), the functions regulated by APE1/Ref-1 include the BER pathway, TFs, energy metabolism, cytoskeletal elements and stress-dependent responses. Thus, APE1/Ref-1 acts as a 'hub-protein' that controls pathways that are important for cell survival. In this review, we will discuss APE1/Ref-1's versatile nature in various human etiologies, including neurodegeneration, cancer, cardiovascular and other diseases that have been linked with alterations in the expression, subcellular localization and activities of APE/Ref-1. APE1/Ref-1 can be targeted for therapeutic intervention using natural plant products that modulate the expression and functions of APE1/Ref-1. In addition, studies focusing on translational applications based on APE1/Ref-1-mediated therapeutic interventions are discussed. ? 2014 KSBMB.
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    New approaches to target cancer stem cells: Current scenario
    (2014) Insan, Mayank Bashyal; Jaitak, Vikas; Insan, M.B.; Jaitak, V.
    Resistance towards chemotherapy and radiotherapy as well as relapse of cancer is the major obstacle in the treatment of cancer. The main factor behind is cancer stem cells (CSCs) which are more resistant to conventional chemotherapy, radiotherapy and are quite able to regenerate whole new tumor again if remain alive during treatment. Targeting CSCs along with actively dividing cancer cells may significantly contribute to the solution of the problem of resistance and relapse. Various approaches are implemented to eradicate CSCs which include CSC markers specific compounds, Drugs which disturb niche and various inhibitors/modulators of signaling pathways. Hedgehog (Hh), Wnt and Notch pathways are modulated/inhibited using various agents and shown beneficial results in multiple forms of cancer. Many inhibitors/modulators of these pathways have been entered in the clinical trials. MicroRNAs have also been developed as anti CSCs agents. In this review, we have covered current status of CSC targeting therapy based on CSC markers, CSC niche, Hedgehog, Wnt, Notch pathway along with MicroRNA based targeting strategies and possibility of implementation multi-targeted anti-CSC therapy for the better outcome of the results. ? 2014 Bentham Science Publishers.
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    An in vitro study ascertaining the role of H2O2 and glucose oxidase in modulation of antioxidant potential and cancer cell survival mechanisms in glioblastoma U-87 MG cells
    (Springer New York LLC, 2017) Cholia, Ravi P.; Kumari, Sanju; Kumar, Saurabh; Kaur, Manpreet; Kaur, Manbir; Kumar, Raj; Dhiman, Monisha; Mantha, Anil K.
    Glial cells protect themselves from the elevated reactive oxygen species (ROS) via developing unusual mechanisms to maintain the genomic stability, and reprogramming of the cellular antioxidant system to cope with the adverse effects. In the present study non-cytotoxic dose of oxidants, H2O2 (100??M) and GO (10??U/ml) was used to induce moderate oxidative stress via generating ROS in human glioblastoma cell line U-87 MG cells, which showed a marked increase in the antioxidant capacity as studied by measuring the modulation in expression levels and activities of superoxide dismutase (SOD1 and SOD2) and catalase (CAT) enzymes, and the GSH content. However, pretreatment (3?h) of Curcumin and Quercetin (10??M) followed by the treatment of oxidants enhanced the cell survival, and the levels/activities of the antioxidants studied. Oxidative stress also resulted in an increase in the nitrite levels in the culture supernatants, and further analysis by immunocytochemistry showed an increase in iNOS expression. In addition, phytochemical pretreatment decreased the nitrite level in the culture supernatants of oxidatively stressed U-87 MG cells. Elevated ROS also increased the expression of COX-2 and APE1 enzymes and pretreatment of Curcumin and Quercetin decreased COX-2 expression and increased APE1 expression in the oxidatively stressed U-87 MG cells. The immunocytochemistry also indicates for APE1 enhanced stress-dependent subcellular localization to the nuclear compartment, which advocates for enhanced DNA repair and redox functions of APE1 towards survival of U-87 MG cells. It can be concluded that intracellular oxidants activate the key enzymes involved in antioxidant mechanisms, NO-dependent survival mechanisms, and also in the DNA repair pathways for glial cell survival in oxidative-stress micro-environment. ? 2017, Springer Science+Business Media, LLC.