School Of Basic And Applied Sciences

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Author: search.filters.author.Kaur S.Has files: No

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    A panoramic review of IL-6: Structure, pathophysiological roles and inhibitors
    (Elsevier Ltd, 2020) Kaur S.; Bansal Y.; Kumar R.; Bansal G.
    Interleukin-6 (IL-6) is a pleiotropic pro-inflammatory cytokine. Its deregulation is associated with chronic inflammation, and multifactorial auto-immune disorders. It mediates its biological roles through a hexameric complex composed of IL-6 itself, its receptor IL-6R, and glycoprotein 130 (IL-6/IL-6R/gp130). This complex, in turn, activates different signaling mechanisms (classical and trans-signaling) to execute various biochemical functions. The trans-signaling mechanism activates various pathological routes, like JAK/STAT3, Ras/MAPK, PI3K–PKB/Akt, and regulation of CD4+ T cells and VEGF levels, which cause cancer, multiple sclerosis, rheumatoid arthritis, anemia, inflammatory bowel disease, Crohn's disease, and Alzheimer's disease. Involvement of IL-6 in pathophysiology of these complex diseases makes it an important target for the treatment of these diseases. Though some anti-IL-6 monoclonal antibodies are being used clinically, but their high cost, only parenteral administration, and possibility of immunogenicity have limited their use, and warranted the development of novel small non-peptide molecules as IL-6 inhibitors. In the present report, all molecules reported in literature as IL-6 inhibitors have been classified as IL-6 production, IL-6R, and IL-6 signaling inhibitors. Reports available till date are critically studied to identify important and salient structural features common in these molecules. These analyses would assist medicinal chemists to design novel and potent IL-6 production and signaling inhibitors, through knowledge- and/or computer-based approaches, for the treatment of complex multifactorial diseases.
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    Alternate mild drought stress (−0.1 MPa PEG) immunizes sensitive chickpea cultivar against lethal chilling by accentuating the defense mechanisms
    (Polish Academy of Sciences, 2016) Kaur S.; Jairath A.; Singh I.; Nayyar H.; Kumar S.
    The changes in climate particularly, the rise in temperature and humidity affect the physiological functions of plants subsequently affecting crop productivity adversely. A strategy is required which can be directly implemented in fields to induce the tolerance in crop plants. In present study, two chickpea varieties with contrasting sensitivity PDG3 (Tolerant) and GPF2 (Sensitive) were raised hydroponically, preconditioned with mild drought stress (0.1 MPa PEG-6000) for 3 days (above 0.1 MPa is lethal) and subsequently recovered for double time (6 days) and finally exposed to lethal cold stress (4 °C) for 3 days. We hypothesize that preconditioning with non-lethal drought stress may immunize the plants to combat lethal cold stress. Membrane integrity improved in root and shoot, lipid peroxidation decreased to control level in preconditioned seedlings. Cellular respiration ability (% TTC reduction) increased in the preconditioned seedlings to almost 90 % in the shoot and 60 % in the root, concurrently it was 45 % in non-preconditioned seedlings. Proline content also increased in preconditioned seedlings, especially roots. Carbohydrate had a shift in terms of a high amount of total, reducing sugars and starch in non-preconditioned seedlings compared to preconditioned. Both PDG3 and GPF2 showed enhanced SOD, CAT and GPOX activity indicating tolerance against cold-induced oxidative stress and preconditioning induced improvement against lethal cold stress.
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    Phytochemical Ginkgolide B Attenuates Amyloid-? amage and Altered Cellular Responses in Human Neuroblastoma SH-SY5Y Cells
    (IOS Press, 2017) Gill I.; Kaur S.; Kaur N.; Dhiman, Monisha; Mantha, Anil K.
    Oxidative stress is an upsurge in reactive oxygen/nitrogen species (ROS/RNS), which aggravates damage to cellular components viz. lipids, proteins, and nucleic acids resulting in impaired cellular functions and neurological pathologies including Alzheimer's disease (AD). In the present study, we have examined amyloid-? (A?)-induced oxidative stress responses, a major cause for AD, in the undifferentiated and differentiated human neuroblastoma SH-SY5Y cells. A?1-42-induced oxidative damage was evaluated on lipids by lipid peroxidation; proteins by protein carbonyls; antioxidant status by SOD and GSH enzyme activities; and DNA and RNA damage levels by evaluating the number of AP sites and 8-OHG base damages produced. In addition, the neuro-protective role of the phytochemical ginkgolide B (GB) in countering A?1-42-induced oxidative stress was assessed. We report that the differentiated cells are highly vulnerable to A?1-42-induced oxidative stress events as exerted by the deposition of A? in AD. Results of the current study suggest that the pre-treatment of GB, followed by A?1-42 treatment for 24, displayed neuro-protective potential, which countered A?1-42-induced oxidative stress responses in both undifferentiated and differentiated SH-SY5Y neuronal cells by: 1) hampering production of ROS and RNS; 2) reducing lipid peroxidation; 3) decreasing protein carbonyl content; 4) restoring antioxidant activities of SOD and GSH enzymes; and 5) maintaining genome integrity by reducing the oxidative DNA and RNA base damages. In conclusion, A?1-42 induces oxidative damage to the cellular biomolecules, which are associated with AD pathology, and are protected by the pre-treatment of GB against A?-toxicity. Taken together, this study advocates for phytochemical-based therapeutic interventions against AD.