ABSTRACT
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 ( P0.05 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.
ABSTRACT
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.
ABSTRACT
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.