1.Changes of heart function and serum cardiac troponin I in early type 2 diabetic rats
Maoshan YIN ; Shuhong XU ; Yanling MU
Chinese Journal of Pathophysiology 2015;(9):1709-1714
AIM:To observe the changes of heart function and the expression of serum cardiac troponin I ( cT-nI) in early type 2 diabetic rats, and to explore the role of cTnI in the development of type 2 diabetes and early diabetic cardiomyopathy .METHODS:The type 2 diabetes rat model was established by an injection of streptozotocin after high fat diet (5 weeks).The rats were randomly divided into control group , model group of 2 weeks, and model group of 4 weeks. M-mode echocardiography was performed for echocardiographic measurements .Fasting blood glucose ( FBG) , total choles-terol ( TC) , triglyceride ( TG) , high density lipoprotein-cholesterol ( HDL-C) , low density lipoprotein-cholesterol ( LDL-C) , fasting insulin ( FINS) and cTnI levels were tested .HE staining was used to observe the pathological changes of myo-cardial structures .The alteration of cTnI in myocardium was determined by Western blot .RESULTS:Compared with nor-mal group , the levels of TC , TG and LDL-C in type 2 diabetic rats were significantly increased , HDL-C levels were signifi-cantly reduced .Cardiac histological analysis revealed that type 2 diabetes induced cardiomyocytes degeneration and necro-sis.The expression of cTnI increased significantly in diabetic groups compared to control group , and that in model group of 4 weeks increased far more than that in model group of 2 weeks (P<0.05).CONCLUSION:The increased level of cTnI and the change of the heart function may be associated with the development diabetic cardiomyopathy .These changes are valuable for the early clinical diagnosis of myocardial injury in diabetic cardiomyopathy .
2.Effects of tetramethylpyrazine-2′-O-sodium ferulate on swelling of astrocytes and expression of AQP4 after oxygen-glucose deprivation/reoxygenation
Shuhong XU ; Maoshan YIN ; Yulin WU
Chinese Pharmacological Bulletin 2015;(12):1661-1666,1667
Aim To explore the effects of tetrameth-ylpyrazine-2′-O-sodium ferulate (TSF)on the swelling of
astrocytes and the expression of AQP4 after oxygen gl-ucose deprivatio /reoxygenation(OGD /Reox).Methods
Astrocytes were divided into 4 groups:control group, OGD /Reox group,Ozagrel group and TSF group.The effects of TSF on astrocytes were investigated 6,1 2,24 and 48 h after OGD /Reox.The cell injury was assessed by measuring LDH activity and MTT.The expression levels of AQP4 protein of astrocytes were detected u-sing Western blot.Results OGD /Reox induced obvi-ous cell swelling and significant reduction of LDH in astrocytes whereas TSF remarkably attenuated OGD-in-duced astrocyte swelling and LDH reduction (P <0.01 ).The expression levels of AQP4 protein in-creased gradually to the peak at 48 h in OGD /Reox
group(P <0.05 ).AQP4 protein levels in TSF group were much lower compared with OGD /Reox group at each time point (P <0.05).And there was no signifi-cant difference between TSF group and OGD /Reox group(P >0.05 ).Conclusion TSF can attenuate OGD-induced swelling of astrocytes through decreasing the AQP4 expression.
3.Alteration of Wnt/β-catenin signaling pathway in early diabetic rat myocardium
Xiaohui XI ; Fuwen WANG ; Yan WANG ; Maoshan YIN ; Yanling MU
Chinese Pharmacological Bulletin 2015;(3):363-366
Aim To investigate the alteration of Wnt/β-catenin signaling pathway in early diabetic rat myo-cardium and clarify its role in development of diabetic cardiomyopathy. Methods The diabetes mellitus ( DM) model was prepared by intraperitoneal injection of streptozotocin ( STZ, 60 μg · g-1 ) . The alteration of Wnt/β-catenin signaling pathway was determined by Western blot and immunohistochemistry. HE staining was used to analyze the change of myocardial pathologi-cal structure. Results Cardiac histological analyses revealed that DM induced cardiomyocyte degeneration and necrosis. Myocardial Wnt2, β-catenin and c-Myc were enhanced in 2 wk DM compared with control group while DKK1 showed no significant alteration. Conclusion Wnt/β-catenin signaling pathway is acti-vated in early diabetic myocardial injury. Further re-searches on its role in DM myocardium may find a new therapeutic target for diabetic cardiomyopathy.
4.Alteration of Wnt/β-catenin signaling pathway in type2 diabetic rats’ aorta and regulation of SIRT1
Maoshan YIN ; Shuhong XU ; Yan WANG ; Xiaohui SUN ; Chen LIANG ; Jie LI ; Yanling MU
Chinese Pharmacological Bulletin 2016;32(3):337-342
Aim To investigate the alteration of Wnt/β-catenin signaling and sirtuins 1 in type 2 diabetic rats’ aorta and clarify its role in the development of di-abetes aortic disease. Methods The type 2 diabetes rat model was established by injection of streptozocin after five-week of high fat diet. The rats were randomly divided into control group, DM model group of 2 weeks, 4 weeks, 8 weeks and 12 weeks. Fasting blood glucose ( FBG ) , total cholesterol ( TC ) , triglyceride ( TG) , high density lipoprotein-cholesterol( HDL-C) , low density lipoprotein- cholesterol ( LDL-C ) and fast-ing insulin( FINS) levels were tested. HE staining was used to observe the pathological changes of aortal struc-tures. The alteration of Wnt2, β-catenin, TCF4, SIRT1 and sFRP2 in aortawas determined by Western blot and RT-PCR. Results Compared with control group, TC, TG, LDL-C levels of type 2 diabetic rats were significantly increased, HDL-C levels were signif-icantly reduced( P<0. 01 ) . Aortic histological analy-sis revealed that DM induced aortic endothelial cell vacuolar degeneration and necrosis. The expression of Wnt2 and β-catenin level increased significantly in the first 4 weeks of diabetic groups compared to control group, and that in model group of 8 weeks and 12 weeks kept in the high level and showed no significant alteration(P>0. 05). But the expression of TCF4 and SIRT1 was enhanced continuously in DM compared with control group while sFRP2 decreased in the duration of DM development. Conclusions Wnt/β-catenin signa-ling pathway was activated in diabetic aortal injury by regulation of SIRT1 via sFRP2 . Further researches on its mechanism of actionin DM aorta injury may find a new therapeutic target for the disease.