Protective Role of Polydatin Against Inflammation and Apoptosis Induced by Hydrogen Peroxide-Induced Oxidative Stress in C6 Cells
Chapter from the book: Bilgili, A. (ed.) 2024. Academic Research and Evaluations in Health Sciences II.

Ahmet Ozan Kaleci
Sivas Cumhuriyet University
Serkan Kapancık
Sivas Cumhuriyet University

Synopsis

Gliomas are tumors that arise as a result of changes in gene expressions as a result of DNA mutations in glial cells in the central nervous system. C6 cell lines from rats are widely used for experimental investigations of biochemical mechanisms in glioma tumors and glial cells. Polydatin is the active molecule obtained by extraction from the root tissue of a plant called Polygonum cuspidatum. Polydatin has pharmacological anti-inflammatory and anti-oxidative properties. The formation of free radicals in our metabolism and the elimination of these radicals are in balance. Thus, no pathological condition is encountered. However, as a result of a high rate of increase in the rate of free radicals or insufficient antioxidant defense systems, a situation in which the balance is disturbed occurs and causes many pathological conditions from cancer to signal transmission disorders in neurons. In our study, we aimed to reveal the protective effect of polydatin against oxidative stress induced by shifting the oxidant-antioxidant balance to the oxidant side via hydrogen peroxide in C6 cell lines by regulating inflammation and apoptosis. As a result, we found that polydatin application revealed a protective effect against cellular damage caused by oxidative stress by re-regulating the expressions of genes related to inflammation and apoptosis in C6 cells.

How to cite this book

Kaleci, A. O. & Kapancık, S. (2024). Protective Role of Polydatin Against Inflammation and Apoptosis Induced by Hydrogen Peroxide-Induced Oxidative Stress in C6 Cells. In: Bilgili, A. (ed.), Academic Research and Evaluations in Health Sciences II. Özgür Publications. DOI: https://doi.org/10.58830/ozgur.pub566.c2768

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Published

December 22, 2024

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