Objective To establish a Goto-Kakizaki ( GK) rat model of duodenal-jejunal bypass( DJB) and ob-serve the changes in insulin-resistance after surgery, and to explore the mechanism of DJB surgery in treatment of type 2 di-abetes mellitus.Methods Male Goto-kakizaki diabetic rats(GK,n=36)were used as experiment group and 18 healthy male Wistar rats as blank group.GK rats were randomly divided into two groups: diabetic control group and DJB surgery group ( n=18) .Euglycemic-hyperinsulinemic clamp technique was performed in 6 rats randomly taken from each group at third week, sixth week and ninth week after surgery, respectively.The expression levels of Gck, G6P, PEPCK mRNA in the liver and GLUT4 content on skeletal muscle cell plasma membrance were detected one week after the clamp test. Results In the DJB surgery group at the end of third week and sixth week after surgery, the levels of glucose infusion rates and the expression levels of Gck, G6P, PEPCK mRNA in the liver showed no statistically significant difference as com-pared with the diabetic control group (P>0.05).In the DJB surgery group at the end of 9th week after surgery, the glu-cose infusion rate and expression level of Gck mRNA in the liver were significantly higher, and the expression of G6P and PEPCK mRNA was significantly lower than those in the diabetic control group ( P<0.05 for all) .At the three time points (3rd week, 6th week and 9th week after surgery), there was no significant difference in the GLUT4 content on skeletal muscle cell plasma membrane between the diabetic control group and DJB surgery group ( P>0.05 for all) .Conclusions Our results indicate that the mechanism of DJB surgery improving blood glucose level may be closely related to the amel-ioration of insulin-resistance in the liver, thereby augmenting glucose uptake and inhibiting gluconeogenesis in liver through the regulation of glucose metabolism-related enzymes.There is no significant improvement in insulin-resistance in the skele-tal muscles during the experiment period.This result implies that the effect of DJB surgery on type 2 diabetes is related to the duration of therapy.

Objective To investigate the protective effects of alpha-lipoie acid (ALA) against beta-cell damage in streptozotocin (STZ)-induced diabetes in rats. Methods Thirty SD rats were randomly divided into three groups: normal control (NC) group, STZ group and ALA + STZ group, with 10 rats in each group. mg/kg, intraperitoneal injection), till the end of the study (4 weeks later). Blood glucose were measured every 3 days after STZ injection. Malondialdehyde (MDA) and reduced glutathione (GSH) levels were measured in pancreatic homogenates. Pancreatic beta-cells were examined by immunohistocbemical methods, Results STZ induced a significant increase of the level of blood glucose. Body weight of rats in ALA + STZ group was (341±26)g, which significantly lower than (368±3)g in NC group, and high than (301±2)g in STZ group with stas(P < 0. 05). Meanwhile the MDA levels in STZ group and NC group were(1.22 ± 0. 14) and(0.57 ± 0.04)nmoL/mg prot, respectively, and there was significant difference between the two groups (P < 0.05) ; the GSH levels in STZ group and NC group were(16.54 ± 1.10) and(25.46 ± 0.62) mg/g prot (P < 0.05), respectively; degeneration of islet cells and decreased blood glucose were observed in STZ + ALA-pretreated rats; MDA level in pancreatic homogenates was(0.72 ± 0. 23)nmoL/mg prot, which was significantly lower than that in STZ group (P < 0.05) ; the GSH level was (35.33 ± 2.66) mg/g prot, which was significantly higher than that in STZ group (P < 0.05) ; increased staining of insulin and preservation of islet ceils functions were more obvious in the STZ + ALA-pretreated rats. Conclusions ALA exerted its protective effect through reducing the oxidative stress and preserving pancreatic beta-cell integrity.

This study examined the anti-viral effect of ursolic acid on guinea pig cytomegalovirus (GPCMV) and explored the steps of viral replication targeted by ursolic acid. Cytopathic effect assay and MTT method were employed to determine the 50% cellular cytotoxicity (CC(50)), 50% effective concentration (EC(50)) and therapeutic index (TI) with GPCMV. To investigate the specific anti-viral effect of ursolic acid at different temperatures and time points, two other medicines, ganciclovir and Jinyebaidu (JYBD), serving as controls, were studied for comparison. Our results showed that the CC50 of ganciclovir, JYBD and ursolic acid were 333.8, 3015.6, 86.7 μg/mL, respectively; EC(50) of ganciclovir, JYBD and ursolic acid was 48.1, 325.5 and 6.8 μg/mL, respectively; TI of ganciclovir, JYBD and ursolic acid was 7, 9, 13, respectively. Similar with ganciclovir, ursolic acid could inhibit the viral synthesis, but did not affect the viral adsorption onto and penetration into cells. We are led to conclude that the anti-cytomegalovirus effect of ursolic acid is significantly stronger than ganciclovir or JYBD, and the cytotoxic effect of ursolic acid lies in its ability to inhibit viral synthesis.

This study examined the anti-viral effect of ursolic acid on guinea pig cytomegalovirus (GPCMV) and explored the steps of viral replication targeted by ursolic acid. Cytopathic effect assay and MTT method were employed to determine the 50% cellular cytotoxicity (CC(50)), 50% effective concentration (EC(50)) and therapeutic index (TI) with GPCMV. To investigate the specific anti-viral effect of ursolic acid at different temperatures and time points, two other medicines, ganciclovir and Jinyebaidu (JYBD), serving as controls, were studied for comparison. Our results showed that the CC50 of ganciclovir, JYBD and ursolic acid were 333.8, 3015.6, 86.7 μg/mL, respectively; EC(50) of ganciclovir, JYBD and ursolic acid was 48.1, 325.5 and 6.8 μg/mL, respectively; TI of ganciclovir, JYBD and ursolic acid was 7, 9, 13, respectively. Similar with ganciclovir, ursolic acid could inhibit the viral synthesis, but did not affect the viral adsorption onto and penetration into cells. We are led to conclude that the anti-cytomegalovirus effect of ursolic acid is significantly stronger than ganciclovir or JYBD, and the cytotoxic effect of ursolic acid lies in its ability to inhibit viral synthesis.
Animals ; Antiviral Agents ; pharmacology ; Cells, Cultured ; Guinea Pigs ; Roseolovirus ; drug effects ; Triterpenes ; pharmacology