Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral isch- emia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb 1, an active component of ginseng, and cortical neurons. Ginsenoside Rb l protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rbl inhibited levels of tumor necrosis factor-a in a co-culture system containing activated N9 microglial cells. Ginse-noside Rbl also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rbl attenuates damage to cerebral cortex neu-rons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-a expression in hypoxia-activated microglia.

Synergistic use of geniposide and baicalin on BV2 cell activation damage caused by LPS

OBJECTIVE To explore the synergistic effect of baicalin and geniposide(BG)on BV2 cell activation damage caused by lipopolysaccharide(LPS).METHODS BV2 murine microglial cell line was cultured in vitro,LPS(final concentration 500 ng·m L-1)and various concentrationof Baicalin and Geniposide(BG)(final concentration12.5,25 and 50μg·m L-1)were added tointerven,the negative control was establised.MTT method was used to value the effect of LPS on the viability of BV2 cell line.The accumulated nitrite was assayed utilizing the Griess reaction method.RESULTS(1)Morphological observation:The common marphological of quesient microglia is circle,cell bodies smaller and synaptic slender.The enlargement of microglial cell bodies and an amoeboid morphology with retraction of extensions are generally induced by LPS.BG markedly suppressed the LPS-activated BV2 microglia morphological variations,meanwhile the dose-dependent was dramaticaly performed.(2)MTT test showed that LPS-stimulated BV2 cells viability was significantly decreased compared to the control group;compared to LPS treated cells,drug group(LPS+BG)effectively improves the LPS-stimulated BV2 cells viability.(3)The Griess reaction method indicated that LPS could obviously promoted the BV2 cells′NO generation contrasted to control group;while the drug group(LPS+BG)can effectively inhibited the generation of NO which activated by LPS.CONCLUSION The treatment group could significantly enhance survival rate of LPSstimulated BV2 cells,while,the level of NO was markedly decreased in BV2 induced by LPS.These findings suggest that combination of BG could attenuate BV2 microglial cells activation and injury which induced by LPS,possessed the capacity of neuroprotective.