EFFECTS OF PUERARIN AGAINST GLUTAMATE EXCITOTOXICITY ON CULTURED MOUSE CEREBRAL CORTICAL-NEURONS

AIM: To study the effects of puerarin (Pue) against injury of cultured neurons by sodium glutamate (Glu). METHODS: Neuronal damage induced b y Glu, N-methyl-D-aspartate (NMDA), and kainic acid (KA), as well as t he actions of Pue and some excitatory amino acid antagonists (EAAA), w ere measured by determining the leakage of lactate dehydrogenase (LDH) from nerve cells. RESULTS: The 24-h leakage of LDH was increased from cells exposed either to Glu 100 and 500 mu mol.L-1 for 15 min (from 2 0 +/- 4 kU/g protein in control group to 35 +/- 3 kU/g protein in Glu 100 mu mol.L-1 group and to 46 +/- 6 kU/g protein in Glu 500 mu mol.L- 1 group) or to NMDA 500 mu mol.L-1 or KA 500 mu mol.L-1 for 45 min (fr om 19 +/- 4 kU/g protein in control group to 27 +/- 3 kU/g protein in NMDA group and to 30 +/- 5 kU/g protein in KA. group). Pre and post-tr eatment with Pue (100 mu mol.L-1) decreased the leakage of LDH, which was similar to the effects of EAAA kynurenic acid (from 35 +/- 3 kU/g protein in Glu 100 mu mol.L-1 to 20 +/- 5 kU/g protein in kynurenic ac id group and to 22 +/- 3 kU/g protein in Pue group), DL-2-amino-5-phos phonovaleric acid (APV) (from 27 +/- 3 kU/g protein in NMDA damaged gr oup to 183 kU/g protein in APV group and to 19 +/- 5 kU/g protein in P ue group) or 6,7-dinitroquinoxaline-2,3(1H, 4H)-diane (DNQX) (from 30 +/- 5 kU/g protein in KA damaged control to 22 +/- 5 kU/g protein in D NQX group and to 20 +/- 4 kU/g protein in Pue group). Post-treatment w ith Pue (100 mu mol.L-1) was able to reduce 24-h leakage of LDH from n eurons expos ed to Glu 100 mu mol.L-1 for 15 min (from 35 +/- 3 kU/g p rotein to 27 1:4 kU/g protein). CONCLUSION: Pue had protective effects on neurons damaged by Glu, NMDA, or KA.