Abstract
The present study monitored the effect of 2, 10, and 50 mg/L of Panax notoginseng saponin exposure following hypoxia-reoxygenation injury in fetal rat cortical neurons. Results showed that varying doses of Panax notoginseng saponin significantly enhanced the cell viability of neurons, reduced malondialdehyde content, increased superoxide dismutase activity, inhibited mRNA and protein expression of inducible and neuronal nitric oxide synthase, and decreased the release of nitric oxide in hypoxia/reoxygenation injured cells. In particular, 50 mg/L of Panax notoginseng saponin was the most effective dose. These findings suggest that Panax notoginseng saponin can attenuate neuronal oxidative stress injury caused by hypoxia/reoxygenation in a dose-dependent manner.
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