Berberine, an isoquinoline alkaloid component of Rhizoma Coptidis has been demonstrated to be the key active ingredient involved in its protective effect against cerebral ischemia-reperfusion. However, the comparison among the analogues to the protective effect against oxygen and glucose deprivation/reoxygenation （OGD-R） was mediated by inhibition of cyclooxygenase-2 （COX-2） has never been reported. The aim of this study is to investigate the protective effect of berberine and its five analogues against OGD-R in PC 12 cells, as well as to determine whether the protective effect was regulated through COX-2. An established in vitro OGD-R model of PC12 cells by oxygen glucose deprivation of 4 h and reperfusion of 24 h was used in our study. After cells were treated with berberine or its five analogues, we examined the cell viability assay by 3-（4,5-dimethylthiazol-2-yl）-2,5- diphenyltetrazolium bromide （MTT） assay. Cells were also collected to determine the levels of mRNA and protein of COX-2 by real time PCR and Western blot. We found that berberine and its analogues improved the viability of PC12 cells against OGD-R. Whereas berberine and berberrubine presented stronger activity with the most effective dose of 0.31 lag/mL and the minimum effective doses of 0.02 and 0.04 gg/mL. Palmatine possessed potentially weaker protective effect. The mRNA level of COX-2 in cells treated with berberine, coptisine and epiberberine was decreased significantly. The protein level of COX-2 was significantly down-regulated in cells treated with berberine. Studies suggested the important role of methylenedioxy groups （R2 and R3） of berberine analogues in COX-2 inhibitory effect, and methylenedioxy groups （R2, R3, R9 and R10） in berberine analogues in binding affinity with COX-2. Substituted hydroxyl group at R9 did not affect the activity of berberine. In summary, our study illustrated the protective effects of berberine and its analogues in PCI2 cells against OGD-R and to elucidate the structure-activity relat
The aims of the present study are to investigate the effect of vasoconstriction and to explore the mechanism of rutae- carpine. The research findings showed that rutaecarpine could induce contractions of the rat thoracic aorta in vitro. The inhibitors of Rho-kinase and inositol 1,4,5-triphosphate receptor （IP 3 R） could suppress the effect of rutaecarpine-induced vasoconstriction. In the study of A7r5 cells （a line of smooth muscle cells）, 300 μg/L rutaecarpine promoted the concentration of intracellular Ca 2＋ and enhanced the IP 3 R expression, which connects with 1,4,5-triphosphate to evoke the release of Ca 2＋ from the intracellular stores. Rutaecarpine increased the RhoA mRNA expression when the cells were pretreated with inhibitor H-1152, and improved the levels of phosphorylation of myosin light chain phosphatase （MLCP） and myosin light chain （MLC）. These results suggest that rutaecarpine plays a role in vasoconstriction relative to the RhoA/MLCP-MLC signaling pathway, which denotes a new field of rutaecarpine in pharmacology.
