Objective: To investigate the biological function of soybean selenoprotein by the study of anti-oxidation,immunological and anticarcinogenic efficacy. Method: The soybean selenoprotein at different doses of Se were fed intra-gastrically in Kunming mice. A low Se feedstuff was used as basic diet. Result: (1) when dose is below 202.5 ?g/kg bw Se, the number of white cell and red cell was increased remarkably, and the activity of GSH-Px and SOD in liver and serum was increased at dose dependent manner, but LPO in serum and liver was decreased noticeably. At level of 607.5?g/kg, all the indices were reversed; (2) A dose-dependent cancer protective effect was expressed in range of 22.5-202.5?g/kg Se of soybean selemoprotein in the diet. Feeding soybean selenoprotein can postpone the death of mice with carcinoma . Total tumour yield was consistently reduced by 78% with 202.5?g/kg supplementation; (3) Any abnormal response was never noticed during all trial by supplementing 202.5?g/kg selenoprotein. Conclusion: The increased effect of anti-oxidation and immunological modulation might be the mechanism of tumour suppression by soybean selenoprotein, and Kunming mice tolerated the soybean selenoprotein very well without any side effects.

AIM:To study the effects and mechanism of peroxisome proliferator-activated receptors(PPARs)ligands,fenofibrate and pioglitazone,on ventricular remodeling in pressure overload rats.METHODS:A pressure overload model was established by the constriction of abdominal aorta in Wistar rats.The hemodynamics and ventricular remodeling parameters,plasma and myocardial renin activity,angiotensin Ⅱ and aldosteron,the mRNA expression of angiotensin Ⅱ type 1 receptor(AT1)were investigated in the constriction of abdominal aorta group(CAA group,n=7)at 12-week after operation and treated experimental groups in which rats were treated with fenofibrate(F group,n=8),pioglitazone(P group,n=7),concomitant fenofibrate and pioglitazone(F+P group,n=6)for 12 weeks since 2 days after operation.The sham-operated rats served as controls(n=8).RESULTS:The ratio of left ventricular weight to body weight,mean arterial pressure,left ventricular systolic pressure,left ventricular end diastolic pressure,left ventricular systolic pressure and heart rate were significantly lower,the maximum left ventricular pressure rising and declining rates(?dp/dtmax)were significantly higher in all treated experimental groups than those in CAA group.Fenofibrate or pioglitazone had no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron.The mRNA expression of AT1 was downregulated in treated groups except F group.CONCLUSION:PPAR ligands have no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron,but fenofibrate and pioglitazone inhibit ventricular remodeling,decrease preload and afterload,increase ?dp/dtmax in pressure overload rats.The expression of mRNA of AT1 is downregulated in myocardium of pressure overload rats by the PPAR? signaling pathway.

To investigate the effect of NVP-DPP728, a DPP-Ⅳ inhibitor on new-onset diabetes and the autoimmune response in non-obese diabetic ( NOD ) mice. Diabetes could be reversed in 75% of NVP-DPP728 treated 20 NOD mice. In these 15 mice with remission, insulitis scores were significantly lower than those of the control group. The percentage of Tregs was increased in the thymus and celiac lymph nodes, plasma TGF-β1 and GLP-1 were also significantly increased ( P＜0. 01 ). NVP-DPP728 treatment may reverse new-onset diabetes in NOD mice by reducing insulitis and increasing Tregs.

Objective To investigate the protective effects of α-1 antitrypsin on human islets injured by protease released from pancreas exocrine cells. Methods ( 1 ) in vivo experiment. Parts of the cadaveric pancreas was digested with collagenase, islets were selected artificially, and pancreatic exocrine cells were collected. 8-9 weeks olds male BALB/c-Nu nude mice were induced into diabetic mice with STZ (240 mg/kg body weight, i. p) and randomly divided into two groups: the control group (n = 6), 250 islets were transplanted into left kidney subcapsule of diabetic nude mice; cotransplant group (n = 7), 250 islets and the equal volume of pancreatic exocrine cells were transplanted into different regions of left kidney subcapsule. Blood glucose level was monitored. Nephrectomies were performed after 28 days. The expression of anti-amylase antibodies in subcapsule was detected by using immunohistochemical staining. (2) Islets culture: Three groups were randomly set up. Group 1: purified islet group, 250 islets were incubated into a 6-well culture plate; Group 2: non-purified islet group, 250 purified islets and equal volume of exocrine cells were incubated; Group 3: nonpurified islet + Al AT group, 250 purified islets and equal volume of exocrine cells were incubated with α-1 antitrypsin added (0. 5 mg/ml). After 48 h, insulin content of islets in each well and trypsin concentration in the supernatant of each well were measured. Results 10000 islets were collected.After islets transplantation, the blood glucose levels in control and co-transplant groups were normal,but a delayed islet function in reversing diabetes was in the co-transplant group, and ehe mice in both groups became hyperglycemic after nephrectomy. A large number of anti-amylase antibody-positive cells were found in renal subcapsule in the co-transplant group while little seen in the control group.Insulin levels in the non-purified islet group were decreased as compared with purified islet group,those in the non-purified islet group + A1AT group were higher than in the non-purified islet group,but lower than in the purified islet groups. Trypsin concentration in the non-purified islet group was increased as compared with purified group, that in the non-purified islet group + A1AT group was lower than the non-purified islet group, but higher than in the purified islets group (all P＜0. 01).Conclusion Protease released from acinar cells during pancreatic digestion has detrimental effect on islet function after transplantation. Co-cultivation of islets and pancreatic exocrine cells with A1AT added can prevent islet cell damage caused by trypsin.