Napabucasin prevents brain injury in neuronal neonatal rat cells through suppression of apoptosis and inflammation

Abstract

The present study investigates the protective effect of napabucasin on the expression of apoptosis markers and inflammatory factors in the neuronal rat cells with post-isolation damage. The level of ROS determined by the fluorescence measurement in the neuronal rat cells with post-isolation damage was 310.21 RFU compared to 21.45 RFU in sham cell cultures. Napabucasin treatment decreased ROS level in the neuronal rat cells with post-isolation damage in dose based manner. ROS level decreased to 278.67, 203.65, 163.32 and 26.87 RFU, respectively in 1, 2, 3 and 4 μM napabucasin treated cell cultures. Treatment with napabucasin increased GSH level significantly (P < 0.05) in the neuronal rat cells with post-isolation damage. Napabucasin treatment at with 1, 2, 3 and 4 μM concentrations increased SOD activity to 2.4, 3.6, 5.1 and 6.1 U/mg, respectively. Treatment with napabucasin increased the activity of catalase in dose based manner. Napabucasin treatment increased Gpx in injured brain cells of neonatal rats. A significant (P < 0.05) increase in the activity of AChE was observed in neuronal rat cells with post-isolation damage on treatment with napabucasin. Treatment with napabucasin reduced the level of TNF-α and IL-6 significantly (P < 0.05) compared to untreated group. Napabucasin treatment decreased the expression of Bax, caspase-3 and p53 proteins in the neuronal rat cells with post-isolation damage. Napabucasin treatment protects post-isolation damage in the neuronal cells of neonatal rats by suppression of apoptosis and oxidative stress. Therefore, napabucasin can be used for the treatment of brain injury.