Investigation of the protective effects of chrysin against paclitaxel-induced oxidative stress and apoptosis in human neuronal SH-SY5Y cells

Paclitaxel is a preventive medicine used to treat various cancers. Paclitaxel works by interfering with the normal function of microtubules, which are key structures in the cell structure. Paclitaxel disrupts the mitotic shell by stabilizing microtubules and preventing them from disintegrating during cell structures, leading to death of the rapidly dividing cancer body. The main groups of anti-cancer organisms are the directing of cancer growth to apoptotic pathways through the production of oxygen species (ROS). However, these produced ROS can cause effects on various tissues and organs, especially neurological, by attacking other countries as well as cancer formations. Their nervous system is much more sensitive to toxic agents due to their class and substances on an effective vascular barrier. It does not have enzymatic and non-enzymatic protective defense against ROS stored under normal conditions. However, the antioxidant defense systems that protect the nerves are quite weak. This leaves them against oxidative stress. For this reason, it was thought that it could be an effective option against drug therapy in nerve cells. The aim of this study was to evaluate the possible protective effects of chrysin against paclitaxel-induced action in SH-SY5Y cells as an in vitro model through oxidative damage and apoptosis. In the scope of the study, different doses of paclitaxel were applied to SH-SY5Y cells and 15 and 30 µM paclitaxel cells were those that expanded cell viability and these damages of 500 and 1000 µM chrysin cells were spent. Chrrysin was also used in paclitaxel treated institutions to benefit from the LPO level. Chrysin also decreased caspase 10, caspase 8, caspase 6, p53, and NFKB data, and increased Bcl-2 levels compared to the paclitaxel-treated groups. These output results suggest that suppression of chrysin oxidative stress and apoptotic cell death may be an effective strategy for the treatment of paclitaxel-induced SH-SY5Y cytotoxicity.