AIMTo observe protective effects and involved mechanism of ginsenoside Rb3 on hypoxic/ischemic brain injury, using cultured hippocampal neurons, rat hippocampal slices and intact animals.

METHODS(1) Mice were tightly closed in glasses of 150 ml, and then survival time of them was observed. (2) During simulated ischemia and after reoxygenation, changes of orthodromic population spikes (OPS) in the area CA1 of hippocampal slice were investigated. (3) By using histochemistry, the expressions of NOS in CA1 area of rat hippocampus after hypoxic exposure were observed. (4) Using LDH detection, tests of total NOS, iNOS and cNOS activity, the protective effects of ginsenoside Rb3 were investigated on cultured hippocampal neurons treated with hypoxia.

RESULTS(1) Given ginsenoside Rb3 (10 mmol/L), mice survived significantly longer than that of control group. (2) The occurrence of HIP (hypoxic injury potentials) decreased after administration of ginsenosides Rb3 (60 micromol/L) in many slices, while the recovery rate and amplitude of OPS after reoxygenation were significantly higher than those of the control group. (3) In CA1 area of rat hippocampus, NOS-positive neurons increased at the end of 24 h hypoxia and further 24 h reoxygenation, while the number of NOS-positive neurons decreased after treatment with ginsenoside Rb3. (4) The LDH leakage rate of cultured rat hippocampal neurons increased at the end of hypoxia, while it decreased after treatment with Rb3. Moreover the total NOS, especially iNOS activity of these neurons also decreased.

CONCLUSIONGinsenoside Rb3 has a significant protective effect on hypoxic-ischemic injury of neurons, and this involves the stabilization of the cell membrane, the inhibition of the expression and activity of NOS, especially iNOS activity.