Propofol produces neurotoxicity by inducing mitochondrial apoptosis

Propofol is a fast and short-acting intravenous anesthetic widely used in clinical anesthesia and intensive care unit sedation. However, its use can cause abnormal effects on the central nervous system. Thus, the purpose of this study was to investigate the mechanism of propofol on primary hippocampal neuron injury. In addition, we aimed to determine whether a correlation exists between propofol and mitochondrial apoptosis-induced neurotoxicity. Hippocampal neurons cultured for 4 days were exposed to different drugs. The treatment groups were divided according to drug exposure into propofol, a rotenone inhibitor, and a coenzyme Q10 agonist groups. The final concentrations of propofol were 1, 10 and 100 mu M. The content of ATP and reactive oxygen species (ROS) in the neurons of each group were detected using commercial kits in the culture supernatant after 3 h of drug exposure. Western blotting was used to analyze the expression of apoptosis-related proteins. The JC-1 kit was used to detect the mitochondrial membrane potential. The results revealed that, compared with the non-propofol treatment groups, the expression of apoptosis-related proteins, ATP content, and mitochondrial membrane potential were significantly decreased while the ROS content was markedly increased in the propofol treatment group. In conclusion, propofol treatment promoted damage to hippocampal neuronal mitochondria in a dose-dependent manner. This damage may lead to neuronal apoptosis and neurotoxicity by inducing the inhibition of mitochondrial respiratory chain complex I.