Effects of puerarin against glutamate excitotoxicity on cultured mouse cerebral cortical neurons
Abstract
AIM: To study the effects of puerarin (Pue) against injury of cultured neurons by sodium glutamate (Glu).
METHODS: Neuronal damage induced by Glu, N-methyl-D-asparate (NMDA), and kainic acid (KA), as well as the actions of Pue and some excitatory amino acid antagonists (EAAA), were 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 mumol.L-1 for 15 min (from 20 +/- 4 kU/g protein in control group to 35 +/- 3 kU/g protein in Glu 100 mumol.L-1 group and to 46 +/- 6 kU/g protein in Glu 500 mumol.L-1 group) or to NMDA 500 mumol.L-1 or KA 500 mumol.L-1 for 45 min (from 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-treatment with Pue (100 mumol.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 mumol.L-1 to 20 +/- 5 kU/g protein in kynurenic acid group and to 22 +/- 3 kU/g protein in Pue group), DL-2-amino-5-phosphonovaleric acid (APV) (from 27 +/- 3 kU/g protein in NMDA damaged group to 183 kU/g protein in APV group and to 19 +/- 5 kU/g protein in Pue 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 DNQX group and to 20 +/- 4 kU/g protein in Pue group). Post-treatment with Pue (100 mumol.L-1) was able to reduce 24-h leakage of LDH from neurons expos ed to Glu 100 mumol.L-1 for 15 min (from 35 +/- 3 kU/g protein to 27 +/- 4 kU/g protein).
CONCLUSION: Pue had protective effects on neurons damaged by Glu, NMDA, or KA.
Keywords:
METHODS: Neuronal damage induced by Glu, N-methyl-D-asparate (NMDA), and kainic acid (KA), as well as the actions of Pue and some excitatory amino acid antagonists (EAAA), were 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 mumol.L-1 for 15 min (from 20 +/- 4 kU/g protein in control group to 35 +/- 3 kU/g protein in Glu 100 mumol.L-1 group and to 46 +/- 6 kU/g protein in Glu 500 mumol.L-1 group) or to NMDA 500 mumol.L-1 or KA 500 mumol.L-1 for 45 min (from 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-treatment with Pue (100 mumol.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 mumol.L-1 to 20 +/- 5 kU/g protein in kynurenic acid group and to 22 +/- 3 kU/g protein in Pue group), DL-2-amino-5-phosphonovaleric acid (APV) (from 27 +/- 3 kU/g protein in NMDA damaged group to 183 kU/g protein in APV group and to 19 +/- 5 kU/g protein in Pue 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 DNQX group and to 20 +/- 4 kU/g protein in Pue group). Post-treatment with Pue (100 mumol.L-1) was able to reduce 24-h leakage of LDH from neurons expos ed to Glu 100 mumol.L-1 for 15 min (from 35 +/- 3 kU/g protein to 27 +/- 4 kU/g protein).
CONCLUSION: Pue had protective effects on neurons damaged by Glu, NMDA, or KA.