Aim To study the effect of saikogenin d (SGD) on prostaglandin E 2(PGE 2) production in C 6 rat glioma cells. Methods Radioimmunoassay was applied to determine PGE 2 production in the cells. Scintillation counting was used to measure liberation of -arachidonic acid (AA) from the cells labeled with -AA. Results In vitro, SGD alone at 1～20 ?mol?L -1 did not affect PGE 2 release from cells, but inhibited its release induced by A23187, a Ca 2+ ionophore. The inhibition was concentration-dependent, with the IC 50 value of about 3 ?mol?L -1. SGD (2～10 ?mol?L -1 ) had no inhibitory effect on A23187-induced AA release or on the conversion of AA to PGE 2 in microsomal preparations. Conclusion SGD inhibites A23187-induced PGE 2 production in C 6 rat glioma cells in vitro, without either inhibition of free AA liberation or a direct inhibition of cyclooxygenase (COX) activity.

Objective: To explore the effect of oxidative stress injury on the mechanism of vascular smooth muscle cell (VSMC) calciifcation induced by calcium and phosphorus in experimental rats.
Methods: The VSMC calcification was induced by incubating the cells with calcium chloride (CaCl2) andβ-sodium glycerophosphate (β-GP) for 8 days, and the cells were divided into 4 groups: ① Control group, ② Calcification group,③ Calciifcation+H2O2 group, ④ Calciifcation+catalase group. The calcium nodule formation and calcium deposition in VSMC were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) was detected by DCFH-DA probe staining and the protein expression of Runx2 was examined by Western blot analysis.
Results: Compared with Control group, Calciifcation group showed the higher ROS production, more calcium nodule and calcium deposition, higher Runx2 protein expression;while compared with Calciifcation group, the above indexes were even higher in Calciifcation+H2O2 group, P<0.05. The ROS production, calcium nodule, calcium deposition and Runx2 protein expression were lower in Calciifcation+catalase group than those in Calciifcation group and Calciifcation+H2O2 group, but still higher than that in Control group. The protein expression of Runx2 was similar between Calciifcation+catalase group and Control group, P>0.05.
Conclusion: CaCl2 andβ-GP treatment may induce VSMC calciifcation via activating ROS-Runx2 signal pathway in experimental rats.

Objective: To explore the effects of Vitamin K2 (VK2) on theaortic artery calciifcation and oxidative stress injury in experimental rats.
Methods: A total of 24 rats were divided into 4 groups:①Control group,②6-week calciifcation group,③12-week calciifcation group and④6-week calciifcation + 6-week VK2 group;n=6 in each group. The arterial calciifcation was induced by warfarin (WFN) treatment. The calcium nodule and deposition in rat’s theaortic artery were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) were measured by DHE probe staining and the morphological changes of mitochondria in smooth muscle cells were detected by transmission electron microscopy.
Results: Calciifcation nodule formed in both 6-week and 12-week calciifcation groups, the calciifcation deposition and ROS were higher than Control group,P<0.01. Compared with both calcification groups, the above indexes were decreased in 6-week calciifcation + 6-week VK2 group,P<0.01. Both calciifcation groups showed mitochondria swelling with unclear structure and cytoplasm vacuoles degeneration in vascular smooth muscle cells. The vascular smooth muscle cell volumes were similar between Control group and 6-week calcification + 6-week VK2 group, and no cytoplasm vacuoles degeneration was observed.
Conclusion: Warfarin induced aortic calciifcation is related to oxidative stress injury which may cause the ultra-micro structural damage in smooth muscle cells; VK2 may reduce the oxidative stress injury and improve the condition of vessel calciifcation in experimental rats.

AIM:To explore the effects of pentoxifylline (PTX) on ventricular remodeling and cardiac function in dilated cardiomyopathy (DCM) rats.METHODS: Lewis rats were randomly allocated to a myocin-induced dilated cardiomyopathy (DCM) group receiving saline (n=10), a DCM group receiving PTX (PTX group; 25 mg?kg-1?d-1, ip, for 30 days, n=10) or healthy control group (n=10). The levels of tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6) and IL-10 in the blood plasma were analyzed by ELISA. The extent of fibrosis was estimated using Masson's staining and immunohistochemistry analyses. Cardiac structure and function were measured by echocardiography.RESULTS: PTX decreased plasma levels of TNF-? and IL-6, and increased IL-10 level in DCM animals compared with DCM group [TNF-?: (7.21?0.24) ?g/L vs (19.30?1.31) ?g/L, P