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.
A series of animal models are used to investigate the anti-depression mechanism of flavonoids in scutellariae radix （SR） in vivo. Depression-like behavior in mice was studied after intraperitoneal administra- tion of SR. The results showed that SR administered to mice by the intraperitoneal route obviously short- ened the duration in the tail suspension test and the forced swimming test, aggravated the symptoms of eyelid ptosis, akinesia, and mortality caused by reserpine, prolonged climbing times, affected the condi- tioned place preference, and increased sugar consumption in mice. However the SR did not affect the head twitches induced by 5-HTP, locomotor activity in mice, the toxicity of yohimbine, and the body temperature decrease caused by high dosage of apomorphine. The tests show that SR has some anti-depression effect related to the dopamine system. Furthermore another anti-depression mechanism was possible that could affect the mechanism of brain reward, bring positive reinforcement, and increase the sensitivity to euphoria in mice.
The invasion of Staphylococcus aureus into respiratory epithelial cells and the followed inflammatory responses cause serious tissue damage.The aim of this study was to investigate the effects of ginsenoside Rg_1（Rg_1）on S.aureus infection in vitro and its action mechanism.An internalization model was constructed to determine the effect of Rg_1 on S.aureus invasion. The changes of expression of integrinβ1,NF-κB and glucocorticoid receptor were analyzed by Western blot.Expression of pro-inflammatory genes was validated using RT-PCR.The results demonstrated that Rg_1 treatment could reduce the invasion of S.aureus into rat pulmonary epithelial cells by down-regulating integrinβ1.Its anti-inflammatory action was exerted through reducing NF-κB and expressions of intercellular adhesion molecule-1（ICAM-1）,tumor necrosis factor-α（TNF-α）,interleukin-2 （IL-2）and interleukin-6（IL-6）.The increased expression of glucocorticoid receptor was involved in this regulation.The results suggested that Rg_1 could play a positive role in reducing S.aureus infections.Rg_1 could be used for the treatment of S.aureus infection,potentially.
