School Of Health Sciences

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    Trans-cinnamaldehyde mitigates rotenone-induced neurotoxicity via inhibiting oxidative stress in rats
    (Elsevier B.V., 2022-12-21T00:00:00) Kumar, Sandeep; Kumar, Sachin; Arthur, Richmond; Kumar, Puneet
    Background: The second most prevalent age-related brain condition, Parkinson's disease (PD) is characterised by the loss of neurons in the substantia nigra pars compacta (SNpc). It is associated with symptoms like bradykinesia, stiffness, tremor, and impaired postural responses. Motor dysfunction, and neurochemical imbalance, are involved in the pathophysiology of PD. It has been hypothesised that trans cinnamaldehyde (TCA) a component of Traditional Chinese Medicine (TCM) can ameliorate Parkinson-like symptoms by altering the levels of different biochemical markers and reverse motor impairments. This research sought to determine the neuroprotective effect of TCA against the neurotoxicity caused by rotenone. Basic Procedure: Rotenone (1.5 mg/kg/day; s.c. for 35 days) was given to rats to induce Parkinson-like symptoms. TCA (5, 10, and 20 mg/kg) and concomitant treatment of TCA (5 mg/kg) with L-NAME (10 mg/kg) were given one hour prior to rotenone administration. Every week until the 35th day, behavioral parameters (muscle coordination, spontaneous motor movement and gait abnormalities) were assessed using rotarod, actophotometer, and narrow beam apparatus respectfully. Rats were decapitated on the 35th day, the striatum and cortex were isolated for biochemical tests. Main findings: Rotenone treatment reduced body weight, altered motor coordination and reduced the oxidative defense system. Treatment with TCA significantly improved the alterations in antioxidant levels as well as behavioral parameters. Furthermore, L-NAME (nitric oxide synthase inhibitor) in combination with TCA had a more significant effect as compared to TCA alone, signifying a possible drug interaction. Principal conclusion: TCA could be employed as an adjuvant in PD management. � 2022 The Authors
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    TcI isolates of Trypanosoma cruzi exploit the antioxidant network for enhanced intracellular survival in macrophages and virulence in mice
    (American Society for Microbiology, 2016) Zago, M.P.; Hosakote, Y.M.; Koo, S.-J.; Dhiman, M.; Pi?eyro, M.D.; Parodi-Talice, A.; Basombrio, M.A.; Robello, C.; Gargc, N.J.
    Trypanosoma cruzi species is categorized into six discrete typing units (TcI to TcVI) of which TcI is most abundantly noted in the sylvatic transmission cycle and considered the major cause of human disease. In our study, the TcI strains Colombiana (COL), SylvioX10/4 (SYL), and a cultured clone (TCC) exhibited different biological behavior in a murine model, ranging from high parasitemia and symptomatic cardiomyopathy (SYL), mild parasitemia and high tissue tropism (COL), to no pathogenicity (TCC). Proteomic profiling of the insect (epimastigote) and infective (trypomastigote) forms by two-dimensional gel electrophoresis/ matrix-assisted laser desorption ionization-time of flight mass spectrometry, followed by functional annotation of the differential proteome data sets (?2-fold change, P<0.05), showed that several proteins involved in (i) cytoskeletal assembly and remodeling, essential for flagellar wave frequency and amplitude and forward motility of the parasite, and (ii) the parasite-specific antioxidant network were enhanced in COL and SYL (versus TCC) trypomastigotes. Western blotting confirmed the enhanced protein levels of cytosolic and mitochondrial tryparedoxin peroxidases and their substrate (tryparedoxin) and iron superoxide dismutase in COL and SYL (versus TCC) trypomastigotes. Further, COL and SYL (but not TCC) were resistant to exogenous treatment with stable oxidants (H2O2 and peroxynitrite [ONOO-]) and dampened the intracellular superoxide and nitric oxide response in macrophages, and thus these isolates escaped from macrophages. Our findings suggest that protein expression conducive to increase in motility and control of macrophage-derived free radicals provides survival and persistence benefits to TcI isolates of T. cruzi. ? 2016, American Society for Microbiology.