Zoology - Master Dissertation

Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/63

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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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    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.