EFFECTS OF TAURINE ON CEREBRAL BLOOD FLOW PERFUSION, CELL APOPTOSIS, AND INFARCT VOLUME IN ACUTE CEREBRAL ISCHEMIC RATS

摘要

Taurine (2-aminoethanesulfonic acid) is one of the most abundant free amino acids in the mammals. This simple non-proteinaceous sulfur-containing amino acid has been thought to be a vital nutrient for development of the immature brain and survival of neural cells (Saransaari and Oja, 2000). Recently, taurine has been shown to be involved in many important physiological functions such as maintaining the structural integrity of the membranes, regulating calcium binding and transport, and functioning as an osmolality regulator, neuromodulator, neurotransmitter, and neuroprotective agent against L-glutamate-induced neurotoxicity (Foos and Wu, 2002). In addition, taurine has been shown to protect neural cells from excitotoxicity and prevent harmful metabolic events evoked by cell-damaging condition such as ischemia or hypoxia and epilepsy (Saransaari and Oja, 2002). Previous studies implied that taurine might be a potential and potent agent against cerebral ischemia. To corroborate its beneficial effects and explore their possible mechanisms, we investigated the effects of taurine on acute cerebral ischemia with respect of cerebral blood flow perfusion, cell apoptosis, neurological deficits and infarct volume.