Taurine protects against bilirubin-induced neurotoxicity in vitro

Kernicterus is a bilirubin-induced encephalopathy in newborn. Its spectrum ranges from subtle extrapyramidal to acute encephalopathy and chronic posticteric sequelae. Current treatment of this serious problem is far from optimal. Taurine has been documented to have protective effects on neuronal cells against ischemia in vivo and in vitro. This study used primary neuronal culture to investigate the toxicological effects of unconjugated bilirubin (UCB) and the protection of taurine against UCB-mediated neuron damage. Dose-dependent reduction of cell viability was found. Changes in neurite outgrowth preceded the reduction of cell viability. The bilirubin-mediated neurotoxicity is mainly due to increased rate of cell apoptosis and higher levels of intracellular free calcium ion level. Taurine dramatically improved cell viability in cultured neurons exposed to 12.5 µM UCB. Taurine pretreatment reduced UCB-mediated apoptotic cell death in primary cultured neurons in a concentration-dependent manner, which was associated with reversal of the increased intracellular free calcium ion levels caused by UCB. This study suggests the potential of taurine as a broad-spectrum agent for preventing and/or treating neuronal damage in neonatal jaundice.