OBJECTIVETo investigate the protective mechanism of geniposide, baicalin and berberine on hypoxia and reoxygenation injury in cultured rat cerebral microvascular endothelial cells.

METHODTo establish a model of hypoxia four hours and reoxygenation twelve hours injury in rat cerebral microvascular endothelial cells in vitro. The injured cells were treated with geniposide (0. 128, 0.064, 0.032 micromol mL(-1), baicalin (0.028, 0.014, 0.007 micromol mL(- 1)) and berberine (0.024, 0.012, 0.006 micromol mL(-1)). The expression of p65 subunit of NF-kappaB was detected by immunocytochemical assay and techniques of image quantitative analysis. The protein expression of NF-kappaB was calculated with the mean optical density and mean area. The nuclear translocation of NF-kappaB was calculated with the percentage of positive cells and ratios of light transmittance of cytoplasm and cell nucleus.

RESULTCompared with the normal group, both the protein expression and the nuclear translocation of NF-kappaB of model group were significant increased (P <0.01). Compared with the model group, the mean optical density of all treated groups was decreased ,but these was no significant difference between them. As compared with model group, the mean area of all treated groups was significant decreased (P < 0.01). The percentage of nuclear translocation of all treated groups is not only lower than that of the model group but higher than that of the normal group (P <0.01). Compared with the model group, the ratios of light transmittance of cytoplasm and cell nucleus of all treated groups was significantly elevated (P <0.01).

CONCLUSIONThe results suggesed that geniposide, baicalin and berberine could protect hypoxia/reoxygenation injuried rat cerebral microvascular endothelial cells injury. One of the mechanism may lie in inhibiting both the protein expression and the nuclear translocation of NF-kappaB.