School Of Basic And Applied Sciences

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    Protective Effect of Hemin Against Experimental Chronic Fatigue Syndrome in Mice: Possible Role of Neurotransmitters
    (Springer, 2020) Thakur, V; Jamwal, S; Kumar, M; Rahi, V; Kumar, P.
    Chronic fatigue syndrome (CFS) is a disorder characterized by persistent and relapsing fatigue along with long-lasting and debilitating fatigue, myalgia, cognitive impairment, and many other common symptoms. The present study was conducted to explore the protective effect of hemin on CFS in experimental mice. Male albino mice were subjected to stress-induced CFS in a forced swimming test apparatus for 21 days. After animals had been subjected to the forced swimming test, hemin (5 and 10 mg/kg; i.p.) and hemin (10 mg/kg) + tin(IV) protoporphyrin (SnPP), a hemeoxygenase-1 (HO-1) enzyme inhibitor, were administered daily for 21 days. Various behavioral tests (immobility period, locomotor activity, grip strength, and anxiety) and estimations of biochemical parameters (lipid peroxidation, nitrite, and GSH), mitochondrial complex dysfunctions (complexes I and II), and neurotransmitters (dopamine, serotonin, and norepinephrine and their metabolites) were subsequently assessed. Animals exposed to 10 min of forced swimming session for 21 days showed a fatigue-like behavior (as increase in immobility period, decreased grip strength, and anxiety) and biochemical alteration observed by increased oxidative stress, mitochondrial dysfunction, and neurotransmitter level alteration. Treatment with hemin (5 and 10 mg/kg) for 21 days significantly improved the decreased immobility period, increased locomotor activity, and improved anxiety-like behavior, oxidative defense, mitochondrial complex dysfunction, and neurotransmitter level in the brain. Further, these observations were reversed by SnPP, suggesting that the antifatigue effect of hemin is HO-1 dependent. The present study highlights the protective role of hemin against experimental CFS-induced behavioral, biochemical, and neurotransmitter alterations. - 2020, Springer Science+Business Media, LLC, part of Springer Nature.
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    Glycyrrhiza glabra (Licorice) root extract attenuates doxorubicin-induced cardiotoxicity via alleviating oxidative stress and stabilising the cardiac health in H9c2 cardiomyocytes
    (Elsevier, 2020) Upadhyay, S; Mantha, A.K; Dhiman, Monisha
    Ethnopharmacological relevance: Doxorubicin (DOX) is an effective anti-neoplastic drug, however; it has downside effects on cardiac health and other vital organs. The herbal remedies used in day to day life may have a beneficial effect without disturbing the health of the vital organs. Glycyrrhiza glabra L. is a ligneous perennial shrub belonging to Leguminosae/Fabaceae/Papilionaceae family growing in Mediterranean region and Asia and widespread in Turkey, Italy, Spain, Russia, Syria, Iran, China, India and Israel. Commonly known as mulaithi in north India, G. glabra has glycyrrhizin, glycyrrhetic acid, isoliquiritin, isoflavones, etc., which have been reported for several pharmacological activities such as anti-demulcent, anti-ulcer, anti-cancer, anti-inflammatory and anti-diabetic. Aim of the study: The objective of the present study is to investigate the interaction between the molecular factors like PPAR-?/? and SIRT-1 during cardiac failure arbitrated by DOX under in vitro conditions and role of Glycyrrhiza glabra (Gg) root extract in alleviating these affects. Materials and methods: In the present study, we have examined the DOX induced responses in H9c2 cardiomyocytes and investigated the role of phytochemical Glycyrrhiza glabra in modulating these affects. MTT assay was done to evaluate the cell viability, Reactive Oxygen Species (ROS)/Reactive Nitrogen Species (RNS) levels, mitochondrial ROS, mitochondrial membrane potential was estimated using fluorescent probes. The oxidative stress in terms of protein carbonylation, lipid peroxidation and DNA damage was detected via spectrophotometric methods and immune-fluorescence imaging. The cardiac markers and interaction between SIRT-1 and PPAR-?/? was measured using Real-Time PCR, Western blotting and Co-immunoprecipitation based studies. Results: The Glycyrrhiza glabra (Gg) extracts maintained the membrane integrity and improved the lipid homeostasis and stabilized cytoskeletal element actin. Gg phytoextracts attenuated aggravated ROS level, repaired the antioxidant status and consequently, assisted in repairing the DNA damage and mitochondrial function. Further, the expression of hypertrophic markers in the DOX treated cardiomyocytes reconciled the expression factors both at the transcriptional and translational levels after Gg treatment. SIRT-1 mediated pathway and its downstream activator PPARs are significant in maintaining the cellular functions. It was observed that the Gg extract allows regaining the nuclear SIRT-1 and PPAR-? level which was otherwise reduced with DOX treatment in H9c2 cardiomyocytes. The co-immunoprecipitation (Co-IP) documented that SIRT-1 interacts with PPAR-? in the untreated control H9c2 cardiomyocytes whereas DOX treatment interferes and diminishes this interaction however the Gg treatment maintains this interaction. Knocking down SIRT-1 also downregulated expression of PPAR-? and PPAR-? in DOX treated cells and Gg treatment was able to enhance the expression of PPAR-? and PPAR-? in SIRT-1 knocked down cardiomyocytes. Conclusions: The antioxidant property of Gg defend the cardiac cells against the DOX induced toxicity via; 1) reducing the oxidative stress, 2) maintaining the mitochondrial functions, 3) regulating lipid homeostasis and cardiac metabolism through SIRT-1 pathway, and 4) conserving the cardiac hypertrophy and hence preserving the cardiomyocytes health. Therefore, Gg can be recommended as a healthy supplement with DOX towards cancer therapeutics associated cardiotoxicity. - 2020
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    Caulerpa taxifolia inhibits cell proliferation and induces oxidative stress in breast cancer cells
    (Springer, 2018) Mehra, Richa; Bhushan, Satej; Yadav, Umesh Prasad; Bast, Felix; Singh, Sandeep
    Caulerpa taxifolia (M. Vahl) C. Agardh or killer alga is known to possess several bioactive secondary metabolites with unique structural modifications. We investigated anti-oxidant and anti-proliferative activity of C. taxifolia extract (CTE) on breast and lung cancer cells, along with possible effects on mitochondrial membrane potential (MMP) and cell cycle progression. The results revealed up to 6-folds increase in reactive oxygen species (ROS), 2-folds increase in glutathione reductase (GR) activity, 1.7-fold increase in superoxide dismutase (SOD) activity and 1.8-fold change in catalase activity w.r.t. untreated cells i.e. 10.72 to 21.44 nmol/min/mL, 2.0 to 3.49 U/mL and 37.51 to 69.26 U/min/g FW, respectively, in MDA-MB-cells. Likewise, selective anti-proliferative activity with IC50 0.19 + 0.1, 0.27 + 0.1, and 0.43 + 0.1 μg/μL, was recorded in MDA-MB-231, T-47D, and H1299 cells. In addition, dose-dependent increase in MMP of up to 40% and G1/S phase mitotic arrest was documented by CTE treatment in MDA-MB-231 cells. The results suggest an anti-proliferative and oxidative stress inducing activity of CTE. Changes in MMP and cell cycle arrest further support the anti-cancer effects of CTE. It is believed that C. taxifolia may be considered as a potent source of anti-cancer drugs, subject to further validations.
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    Role of Helicobacter pylori Enriched Media in Inducing Oxidative Stress in Human Cell lines
    (Central University of Punjab, 2018) Samal, Pallavi; Dhiman, Monisha
    Helicobacter pylori is a gram-negative, helical, microaerophilic bacterium which colonizes the human gastrointestinal tract. Vacuolating cytotoxin A (VacA) is one of the major virulent factors. Reactive oxygen species (ROS) and Reactive nitrogen species (RNS) produced by the immune and epithelial cells damage the host cell thereby resulting in a persistent infection. The prolonged infection results in chronic inflammation, oxidative stress and DNA damage. The microbe affects the major macromolecules of the host tissues lipids, proteins and DNA which leads to lipid peroxidation, protein oxidation and DNA fragmentation hence making the oxidative stress a deleterious damage. Role of H. pylori enriched media (HPEM) in inducing oxidative stress in two human cell lines AGS (human gastric cell line) and THP-1(human monocytic cell line) was studied in present work. The AGS cells and THP-1 cells was treated with various concentrations of HPEM and oxidative stress was evaluated by examining the levels of protein carbonyls, TBARS (thiobarbituric acid reactive species) and nitric oxide by spectophotometric and Western blotting methods. The oxidative stress induced by HPEM showed damaging effects on the cell membrane, protein and produced significantly high nitric oxide (NO) when compared with the untreated controls. From the present work it can be concluded that HPEM exposure to THP-1 and AGS cells enhanced the oxidative stress which leads to cellular damage and is ultimately responsible for the severe H. pylori associated fatal complications during its pathogenesis.
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    Neuro-Protective Role Of Ginkgolide B In A?induced Neurodegeneration And Ache Enzyme Activity In Human Neuroblastoma Sh-Sy5Y Cells
    (Central University of Punjab, 2018) Mukherjee, Ankita; Mantha,Anil K.
    Ginkgolide B (GB) is being used as medicine in China for treating neurodegenerative diseases for a long time. Its neuroprotective role is getting well established. Alzheimer's disease (AD) is a neurodegenerative disease that has multiple factors associated with its onsetand is one of the most common causes of dementia in the world. GB is known to reduce the oxidative stress caused due to accumulation of amyloid beta (A?), a major hallmark of AD associated strongly with the production of oxidative stress via production of ROS. The increase in the expression of AChE has been reported and it has been associated with increased toxicity of A?. This study tried to decipher the relationship between A?, GB and AChE activity. In this study, it was found that A?(25-35)-induced oxidative stress leads to increased production of ROS and decreased AChE activity. On the other hand, GB decreased ROS production and expression of AChE, thus pointing toward its protective effect. GB increased the activity of AChE, suggesting that due to its antioxidant potentialit possibly caused a decrease in protein oxidation, and thus increased the activity of the AChE enzyme. Therefore, the results of the present study show the modulatory role of GB an AChE enzyme activity under oxidative stress conditions as seen in AD, suggesting the potential of GB in AD therapeutics
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    To study the effect of insulin on advanced androgen-indpendent prostate cancer (pc-3) cells
    (Central University of Punjab, 2012) Kumar, Abhimanyu; Kumar, Sanjeev
    Prostate cancer is one of the major causes of mortality in males over the age of fifty all over the world. Many factors including genetics and diet have been associated with the development of prostate cancer. Hyperinsulinemia has been found to be associated with higher risk of Prostate cancer. Diabetes type-2 is accompanied with hyperinsulinemic state. Both cancer and diabetes are metabolic disorders and often diabetes is correlated with cancer. This study reveals that insulin acts as a mitogen hence increases proliferation in PC-3 cells. Reactive oxygen species are by product of cellular metabolism. Insulin treatment increases cellular metabolism due to which ROS level also increases at higher insulin doses. ROS is necessary for many cells signalling process, abnormal increase in ROS level can cause mutational DNA damage and affects protein folding. Antioxidants and free radical balance is critical for normal cellular functioning. Superoxide dismutase is an important antioxidant enzyme, which keeps ROS level low by dismutation of superoxide anion into hydrogen peroxide. This is further metabolised by catalase. In our study we have found that at lower insulin doses SOD level increases but at higher insulin doses SOD expression decreases significantly. This may be the possible reason of ROS increase. Matrix metalloproteinase's expression is modulated by insulin, which can lead to increase in malignancy. All factors stated above indicate that hyperinsulinemia can lead to tumor progression.