Objective:To investigate the effect of acute myocardial infarction (AMI)-activated inflammation on adipokine imbalance and the therapeutic effects of statin.Methods:A total of 32 C57BL/6 mice were divided into 4 groups:a sham group,an AMI group,a low-dose atorvastatin [2 mg/(kg.d)] group and a high-dose atorvastatin [20 mg/(kg.d)] group.AMI models were established by surgical coronary artery ligation.Plasma levels of high sensitive C reaction protein (hs-CRP),adiponectin and resistin were measured.Adiponectin and resistin expressions were determined.In addition,mouse 3T3-L1 preadipocytes in vitro were differentiated and they were stimulated by oxidized low density lipoprotein (ox-LDL).The protein expressions of adiponectin and resistin in adipocytes were detected.The effects of atorvastatin on ox-LDL-induced adipokine imbalance in adipocytes were identified.Results:The plasma levels of hs-CRP and resistin in AMI mice were significantly increased,whereas the plasma levels of adiponectin were remarkably decreased.However,atorvastatin treatment blocked the changes in the plasma levels of hs-CRP,resistin and adiponectin in AMI mice in a dose-dependent manner.Consistent findings regarding the adipose expressions of the two adipokines were obtained.The plasma levels of hs-CRP were positively correlated with resistin but negatively with adiponectin.In vitro study,ox-LDL increased resistin protein and adiponectin expressions in adipocytes,which were dose-dependently reversed by atorvastatin.Conclusion:Inflammation activation in AMI mice leads to adipokine imbalance.Atorvastatin ameliorates the AMI-induced adipokine imbalance via anti-inflammation.

Objective The mutation of the ABCB6 gene is involved in a variety of diseases , including dyschromatosis univer-salis hereditaria (DUH).This study aimed to construct the expression vectors for the ABCB 6-DsRed fusion proteins, pDsRed-wt-AB-CB6 and pDsRed-L356P-ABCB6, detect its cellular localization in A375 cells, and thus facilitate future studies on the pathogenesis of ABCB6-related diseases . Methods The recombinant plasmids pDsRed-wt/L356 P-ABCB6 were constructed based on the previously constructed pIRES2-ZsGreen1-ABCB6 vector and then transfected into A 375 cells.At 48 hours after transfection , the expression of AB-CB6 was detected by Western blot and the cellular localization of ABCB 6 determined under the laser scanning confocal microscope . Results The expression vectors pDsRed-wt/L356P-ABCB6 were verified by colony PCR, enzyme digestion, and DNA sequencing. The expression of ABCB 6 was significantly increased in the A 375 cells after transfected with the recombinant plasmids .Confocal mi-croscopy showed the localization of both wild-type and mutant ABCB6 in the cytoplasm. Conclusion The expression vectors for wild-type and mutant ABCB6-DsRed fusion protein were successfully constructed and the localization of ABCB 6 in A375 cells was de-termined, which may serve as a basis for further studies of ABCB 6 and the pathogenesis of ABCB 6-related diseases .

Objective:To investigate the role of apolipoprotein A5 (apoA5) in the pathogenesis of obesityrelated hypertriglyceridemia and the related therapeutic effects of metformin.Methods:The ob/ob mice were treated with regular chow diet and metformin for 4 weeks,and the levels of hepatic triglyceride (TG) and apoA5 were measured.Hepatic IAR20 cells were treated with metformin and/or apoA5 siRNAs,and then cellular TG contents and apoA5 expression were determined.Results:High plasma and hepatic levels of apoA5 and TG were found in ob/ob mice.The plasma levels of apoA5 were positively correlated with plasma TG in these mice.Metformin could dosedependently decrease the plasma and hepatic levels of apoA5 and TG in ob/ob mice.Metformin could also dose-dependently reduce cellular TG contents and apoA5 expression,these effects were attenuated by knockdown of apoA5.Conclusion:Hepatic apoA5 is up-regulated in ob/ob mice,which contributes to the elevation of plasma TG.Metformin could inhibit hepatic apoA5 expression,leading to the reduction of the plasma level of TG.