Aim To investigate the effects of ecdysterone on insulin sensitivity and glucose metabolism in the insulin resistant HepG2 cell model induced by high concentration of insulin. Methods The insulin-stimulated glucose incorporation rate was determined with ~3H-D-glucose uptake test which was used to estimate insulin sensitivity of HepG2 cell, and glucose consumption, the amounts of glucose disappeared from the culture medium of HepG2 cells within 24 h were determined. Results The incubation of insulin resistance cells with ecdysterone 1?10~ -6 ～10~ -4 mol?L~ -1 could significantly increase the glucose uptake and glucose consumption of the cells compared with that of control cells(P0.05). Conclusion Ecdysterone could improve the insulin sensitivity in the cell model and can attenuate the aggression of insulin resistance. The effect to improve the insulin sensitivity with ecdysterone is similar to that with pioglitazone.

This article reviewed the appli ca tion of molecular biology technology, such as genomics, DNA labeling technology, and DNA microarray. The aim is to provide the reference for the modernization o f Chinese material medica.

Aim To investigate whether ecdysterone is able to exert glucose-lowering effect on hepatocytes or stimulate the secretion of insulin.Methods For glucose consumption studies,the amounts of glucose disappeared from the culture medium of HepG2 cells within 24 h were determined.?TC3 cells were also used to monitor insulin secretion.Results The glucose concentrations decreased significantly by ecdysterone 1?10~(-6)～10~(-4) mol?L~(-1),while glucose consumption increased by 44%～77% with ecdysterone.Glucose consumption declined as its concentrations increased.Insulin had no effect on glucose-lowering of ecdysterone.?TC3 cells were not stimulated by ecdysterone.Conclusion Ecdysterone is able to exert glucose-lowering effect on hepatocytes which is insulin independent,but has no effect on insulin secretion.

Objective To explore the difference of male and female rats in establishing diabetic model by feeding lardy diet and intraperitoneally injecting a low dose streptozotocin(STZ).Methods Totally 184 male and female Wistar rats(each 92 rats) were induced to diabetes mellitus by feeding lardy diet and intraperitoneally injecting 25 mg/kg STZ for 5 weeks.For the 114 left living rats(70 females and 44 males),they were randomized into female high rosiglitazone group(n=23),male high rosiglitazone group(n=15),female low rosiglitazone group(n=23),male low rosiglitazone group(n=15),female model group(n=24),and male model group(n=14).Rosiglitazone at 2 or 0.5 mg/kg were intragastrically administered to corresponding rats once a day for 4 weeks.Another 8 health female and 8 health male rats receiving same volume solvent served as normal control.The body weight,taken food amount,fasting blood glucose,plasma insulin content and the morphology of the spleen were measured and examined to validate the animal models.Results Blood glucose,total plasma lipids and cholesterol of model rats were markedly increased after STZ injection.And there were some other symptoms of model rats,such as polyuria,polydipsia and polyphagia,which indicated that diabetes had been induced in the models.The male model rats had higher mortality,body weight,triglyceride level and lower plasma insulin than in female(P

Objective To investigate some points in evaluating the effects of insulin sensitizer on obesityassociated non-insulin-dependent diabetes mellitus Zucker fa/fa rat model. Methods Total 20 male Zucker fa/fa rats were divided into model group and rosiglitazone groups. Another 10 male Zucker fa/? rats served as normal control. Rosiglitazone at 6 mg/kg was given intragastrically once per day for 4 weeks,and the rats of the other 2 groups were fed with same solvent at same volume. Results Rosiglitazone reduced the levels of fasting insulin,triglyceride ( TG) and free fatty acid ( FFA) of Zucker fa/fa rats ( P

Aim To establish insulin resistant HepG2 cell model induced by high concentration insulin in vitro culture and evaluate the effects of pioglitazone on insulin sensitivity and glucose metabolism in the cell model.Methods HepG2 cells were incubated with 5?10~(-7)mol?L~(-1) insulin for 16 h and insulin-stimulated()~3H-D glucose incorporation was determined.Then,insulin-stimulated glucose incorporation rate which was used to estimate insulin sensitivity of HepG2 cell,and glucose consumption,the amountsof glucose disappeared from the culture medium of HepG2 cells within 24 hours was determined.The insulin resistance cells were incubated with pioglitazone 1?10~(-5) mol?L~(-1).Results It was demonstrated that the incorporation rate of()~3H-D-glucose in insulin-resistant HepG2 cells was decreased significantly than that in the control cells.Insulin-resistant HepG2 cells were free from stimulation for 48 h by insulin,but the incorporation rate of()~3H-D-glucose was lower than that in control cells.Incubation of insulin resistance cells with pioglitazone significantly increased glucose uptake and glucose consumption by the cells compared with that of the control cells(P

Aim To screen alteration in protein level in brain tissue between middle cererbral artery occlusion(MCAO) and the total saponins of Rubus Parviflolius L(TSRP) treated rats and to learn the mechanism of nerve-protecting effects of TSRP after focal cerebral ischemia-reperfusion.Methods The MCAO 2 h reperfusion of 24 h model was established in rats,2-DE was applied to preparein step 1 for the separation of protein,and imaging analysis of gels was done with Image-Master 2D software.Different protein spots expressing between cerebral ischemic reperfusion(CIR) model and TSRP group were cut from the gels for the MS analysis,Different protein spots expressing between cerebral ischemic tissue administered with or without TSRP were also cut from the gels for the MS analysis.MALDI-TOF-MS and database search: protein spots from step 2 were subject to in-gel digestion and MALDI-TOF-MS analysis,which resulted in the peptide mass fingerprint spectra(PMF).PMF were search against swiss-prot database using search program of Ms-Fit.Results By comparative proteome analysis,29 expression-altered spots were excised for MS and informatics analysis,comparing to the CIR model,18 proteins up-regulated in the TSRP group,11 proteins down-regulated,7 spots of them were identified and characterized.Conclusion The protective effect of TSRP on cerebral ischemia-reperfusion is the result of the participation of a number of proteins.

Aim To establish a model of focal cerebral ischemic tissue of rat brain and explore the injury mechanism of focal cerebral ischemia reperfusion in whole level of proteins.Method The model was established with suture method by reperfusion 24 h after ischemic 2 h according to Koizumi′s method,total brain tissue proteins were extracted with Lysis buffer,proteins were separated by two-dimensional electrophoresis(2-DE),stained by Coomassie brilliant blue,the patterns were gotten,differential proteins were found out,PMS was obtained by MALDI-TOF-MS,and related information of proteins was gained by MS-Fit database.Results A comparative proteomic study of model and normal group was performed.Compared with model group,the normal group gained 23 differential protein spots,13 spots expressed lowly,and 10 spots high,6 protein spots were identified,the relative cerebral ischemic proteins such as Leukotriene A-4 hydrolase,Thyrotropin-releasing hormone-degrading ectoenzyme etc were found out.Conclusions Establishing a 2-DE technology is applied to protein analysis of brain tissue,and the relative proteins of cerebral ischemia are found from proteome aspect.This will contribute to the research on the injury mechanism of cerebral ischemic tissues.

Proteomic technology has been widely used in the research of differently-expressed proteins under different physiology and pathologic conditions.In the aspect of the human spermatozoa proteomics,many reports have demonstrated the differently expressed proteins and the roles of sperm under different physiology and pathologic state from proteome level,and these results provided reliable theoretic base for well understanding of sperm molecule mechanism in physiology and pathologic conditions.

Aim To explore the mechanism of neuro-protecting effects of TGRP on ischemic cerebral injury.Methods The middle cerebral artery was occluded for 2 h to produce focal ischemic followed by 24 h reperfusion.HE staining,TUNEL labeling and immunohistochemical methods were used to investigate changes of neuronal apoptosis and expression of the apoptosis-related proteins after administration of TGRP.Result TGRP decreased the pathologic changes significantly.The apoptosis of neural cells and the expression of Bax positive cells in the TGRP groups significantly decreased compared with the control group(P