OBJECTIVE:To study the effects of rosiglitazone(RH)on body weight,FPG,FFA and other indicators in diabe-tes model rabbit. METHODS:18 rabbits were evenly randomized into control group,model group and dextran group. The latter 2 groups were given alloxan intravenously to induce diabetes model. 3 groups were given RH(0.5 mg/kg)intragastrically,and dex-tran group was additionally given dextran 40 glucose injection(5 ml/kg)intravenously,once a day,for consecutive 3 weeks. Body weight,serum level of FPG,FFA,AngⅡ and NO were determined before and after medication. RESULTS:Compared with be-fore medication,body weight of rabbits in control group were increased after medication,while the levels of FFA and AngⅡ were decreased;the levels of FPG and FFA were decreased in model group;body weight of rabbits were decreased in dextran group af-ter medication,with statistical significance (P<0.01 or P<0.05);other indicators had no statistically significant difference (P>0.05). The level of FFA in dextran group was higher than in model group after medication,with statistical significance(P<0.01). CONCLUSIONS:Rosiglitazone can lead to weight gain by a mechanism which reduce the level of FFA.

Objective To explore the value of ocular fundus artery hemodynamics in diabetes by the correlation study between ocular fundus artery and glycosylated hemoglobin(GHb).Methods GHb was checked in 98 patients (196 eyes) in diabetes,including 49 cases (98 eyes) before treatment and 49 cases (98 eyes) after treatment,and normal group of 100 cases (200 eyes)An all cases,color Doppler ultrasonography was used for monitorind ophthalmic artery(OA),central retinal artery(CRA) and posterior ciliary artery (PCA).Finally,the differences of the parameters vauels of the the OA,CRA,and PCA between diabetic and normal group were studied in order to find out the relationship with GHb.Results Of 98 patients in diabetes,peak systolic velocity and end diastolic velocity of fundus artery decreased,resistance index increased(RI).There was significant difference between diabetic and normal group(P ＜0.05),and a significant difference was exited between diabetic group before and after treatment(P ＜0.05).GHb were negatively correlated with the velocity of fundus artery,and positively correlated with RI.Conclusions Evaluation of ocular fundus artery hemodynamics in diabetes can provide useful information for diabetic retinal perfusion and function change.For evaluation of diabetic retinal disease,it is of great value in clinical application.

[ ABSTRACT] AIM:To explore the role of SHARPIN in regulation of Rip1 in castration-resistant prostate cancer LNCaP-AI cells.METHODS:The LNCaP-AI cells were treated with TNF-α+Z-VAD ( an inhibitor of pan-caspase) to activate necroptosis, which were compared to the cells treated with TNF-α+Z-VAD+Nec-1 ( an inhibitor of Rip1 ) .A blank group and a TNF-α-treated group were set up as controls.The cell viability in each group was measured by MTS as-say.In addition, SHARPIN was knocked down by siRNA, and the inhibitory efficiency was evaluated by RT-qPCR.The expression of Rip1 at mRNA and protein levels after knocking down SHARPIN was determined by RT-qPCR and Western blot to explore the underlying mechanism of regulatory network of necroptosis in prostate cancer.RESULTS: Compared with blank control group and TNF-α-treated group, the viability of LNCaP-AI cells treated with TNF-α+Z-VAD decreased by 28%(P<0.05).After treated with TNF-α+Z-VAD+Nec-1, the LNCaP-AI cells showed no significant difference in the viability compared with blank control and TNF-α-treated groups.Taken together, necroptosis may be an important way of cell death in LNCaP-AI cells.Besides, the expression of Rip1 at protein level was up-regulated following the inhibition of SHARPIN using siRNA, indicating that down-regulation of SHARPIN enhanced necroptosis via activating Rip1 in
LNCaP-AI cells.CONCLUSION:Necroptosis is an important way of cell death .Inhibition of oncogenic factor SHARPIN enhances necroptosis via activating Rip1 in LNCaP-AI cells.

[ ABSTRACT] AIM: To investigate the SALL4 expression, proliferation and apoptosis in the LNCaP cells after transfection of SALL4 siRNA.METHODS: The expression of SALL4 at mRNA and protein levels was detected by real-time PCR and Western blotting.MTS assay, colony formation assay and flow cytometry were used to determine the prolifer-ation, colony formation ability and apoptosis of the LNCaP cells.The effect of SALL4 on the expression of Bax and Bcl-2 was analyzed by Western blotting.RESULTS:Compared with negative control group, the expression of SALL4 at mRNA and protein levels in LNCaP cells was down-regulated by transfection of SALL4 siRNA ( P<0.05 ) .The proliferation rate and colony formation ability were decreased, while apoptosis rate increased in si-SALL4 group (P<0.05).Higher expres-sion of Bax and lower expression of Bcl-2 in si-SALL4 group were observed ( P<0.05 ) .CONCLUSION:Down-regula-tion of SALL4 by siRNA not only suppresses LNCaP cell proliferation and colony formation, but also inhibits Bcl-2 expres-sion and activates Bax expression to induce apoptosis.