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.
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Date
2018
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Publisher
Central University of Punjab
Abstract
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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Keywords
Glioblastoma Multiforme (GBM), Monoamine Oxidase (MAO), Oxidative Stress, Curcumin, Amyloid Beta (25-35)
Citation
Behera, Nishibala N (2018) 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.