OBJECTIVE： To investigate the effects of total flavonoids of Jasminum nudiflorum （TFJN） on pancreatic islet function in type 2 diabetes mellitus （T2DM） model mice and its possible mechanism. METHODS： Totally 10 Kunming mice were included in blank group and given normal diet. Other 75 mice were included in model group and given high-lipid and high-glucose diet for 4 weeks combined with streptozotocin once via sublingual vein to induce T2DM model. After modeling， the mice were randomly divided into model group， metformin hydrochloride group （positive control， 350 mg/kg）， TFJN low-dose， medium-dose and high-dose groups （100， 200， 400 mg/kg， by crude drug）， with 10 mice in each group. Blank group and model group were given constant volume of normal saline intragastrically； administration groups were given relevant medicine intragastrically； once a day， for consecutive 6 weeks. The level of fasting dynamic blood glucose was measured after modeling （before medication） and 2， 4， 6 weeks after medication. The histomorphological characteristics of pancreatic tissue were observed by HE staining. The contents of serum insulin （INS）， insulin cell antibody （IAA）， TNF-α， IL-1β， IL-6， IL-18， CRP， leptin （LP） and adiponectin （ADPN） were measured by ELISA. RESULTS： Compared with blank group， islet atrophy， blurred boundary， insufficient cytoplasm and smaller volume of pancreatic tissue were observed in model group. The fasting dynamic blood glucose level （at different time points after medication）， the contents of IAA， TNF-α， IL-1β， IL-6， IL-18， CRP and LP were increased significantly， while the contents of INS and ADPN were decreased significantly （P＜0.01）. Compared with model group， above symptoms of pancreatic tissue in administration groups were relieved， and the fasting dynamic blood glucose level （2， 4， 6 weeks after administration in metform in hydrochloride group， 4， 6 weeks after administration in TFJN groups）， the contents of IAA， TNF-α， IL-1β， IL-6， IL-18， CRP and LP were decreased signifi- cantly， while the contents of INS and ADPN were increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： TFJN can repair the damaged pancreas of mice with T2DM， reduce the level of blood glucose， and improve the sensitivity of the body to insulin， the mechanism of which may be associated with reducing the secretion of inflammatory factors.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective:To evaluate the therapeutic effect of sustained release bistratal drus film containing dexamethasoni acetate (DA) in treatment of oral ulcer. Methods:Totally 667(231 cases as control group) patients (June 1998 to September 2001) with recurrent aphthous ulcer, lichen planus, radio catarrh were studied randomly to evaluate the therapeatic effect in a single blind random way. Results:The effective rates of treated group and control group were 96.1% and 28.6%, respectively, and the difference between 2 groups was significant ( P

Objective:To evaluate the biological safety of the sustained release bistratal drug film of dexamethasoni acetate (DA). Methods:A series of tests, including acute toxicity test, cytotoxity test (agar overlay), oral mucous membrane irritation test and haemolysis test were conducted. Results:Cytotoxic effect was not observed, nor was toxic effect in mouse toxicity test. The haemolysis rate of this material was 0.46%. Local mucous membrane irritation reaction was not found. Conclusion:The drug film of DA shows excellent biocompatibility on the preliminary tests.