Abstract: Objective To investigate the effects of N-acetyl-L-tryptophan (L-NAT) on H2O2-induced apoptosis of primary hippocampal neurons (PHN). Methods The apopotosis modle of PHN, a cellular model of cerebral ischemia, was made by H2O2. Immunofluorescence staining was used to detect the expression of caspase-3, Rhodamine 123 staining was used to detect mitochondrial membrane potential changes, trypan blue staining was used to detect survival rate, the colorimetric assay was used to detect the activity of caspase-3 and LDH, Western blot was used to detect the expressions of caspase-3 and apoptosis-inducing factor and cytochrome C and other mitochondrial pro-apoptotic factor in the cytosolic proteins and mitochondrial proteins. Results L-NAT inhibits H2O2-induced cell death, loss of mitochondrial membrane potential, downstream release of LDH and mitochondrial factors, and activation of caspase-3 in primary hippocampal neurons. Conclusions L-NAT had effectiveness on cerebral ischemia/hypoxia injury though caspase-independent and caspase-dependent apoptosis pathway.

Key words: N-acetyl-L-tryptophan, neuron, ischemia/hypoxia injury, apoptosis, cellular model