ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
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 .