Protective effect of bilobalide against nitric oxide-induced neurotoxicity in PC12 cells
Abstract
"AIM:
To examine the effects of bilobalide on nitric oxide-induced neurotoxicity in pheochromocytoma-derived PC12 cells (PC12 cells).
METHODS:
PC12 cell survival was monitored by LDH release and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. Superoxide dismutases (SOD) and catalase (CAT) activities were measured based on their abilities to inhibit the oxidation of epinephrine by the xanthine-xanthine oxidase system or to decompose H2O2 respectively. The content of malondialdehyde (MDA) was measured by a fluorometric assay to indicate the lipid peroxidation.
RESULTS:
3-Morpholinosydnonimine (SIN-1, 50-300 mumol.L-1) induced PC12 cell damage. After the cells had been pretreated with 10 mumol.L-1 bilobalide for 24 h, the cell viability was increased to 91% +/- 30% from 52% +/- 14% in SIN-1 alone group. Moreover, the activities of SOD and CAT were increased after cells were treated with bilobalide.
CONCLUSION:
The NO-induced neurotoxicity can be protected by bilobalide in PC12 cells. The bilobalide-induced increase in SOD and CAT activities may serve as one of the mechanisms underlying the neuroprotective effect of bilobalide."
Keywords:
To examine the effects of bilobalide on nitric oxide-induced neurotoxicity in pheochromocytoma-derived PC12 cells (PC12 cells).
METHODS:
PC12 cell survival was monitored by LDH release and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. Superoxide dismutases (SOD) and catalase (CAT) activities were measured based on their abilities to inhibit the oxidation of epinephrine by the xanthine-xanthine oxidase system or to decompose H2O2 respectively. The content of malondialdehyde (MDA) was measured by a fluorometric assay to indicate the lipid peroxidation.
RESULTS:
3-Morpholinosydnonimine (SIN-1, 50-300 mumol.L-1) induced PC12 cell damage. After the cells had been pretreated with 10 mumol.L-1 bilobalide for 24 h, the cell viability was increased to 91% +/- 30% from 52% +/- 14% in SIN-1 alone group. Moreover, the activities of SOD and CAT were increased after cells were treated with bilobalide.
CONCLUSION:
The NO-induced neurotoxicity can be protected by bilobalide in PC12 cells. The bilobalide-induced increase in SOD and CAT activities may serve as one of the mechanisms underlying the neuroprotective effect of bilobalide."