Abstract:
Objective To investigate protective effect and mechanism of mangiferin on myocardial injury in diabetic rats.
Methods Fifty Sprague-Dawley(SD)rats were randomly divided into five groups:a normal control group,a diabetic model group,and groups of low,moderate,and high does mangiferin.The diabetic model was established with tail vein injection of streptozocin(45 mg/kg).Mangiferin at the does of 15,30,60 mg/kg·d were given to the rats for 12 weeks.Blood glucose,cardiac mass index,left ventricular mass index and heart function of the rats were measured;cardiac pathological changes were observed with hematoxylin-eosin staining;immunohistochemical method was used to detect expressions of activator protein-1(Ap-1),transforming growth factor-β
1(TGF-β
1),and fibronectin(FN)in myocardial tissue of the rats.
Results Compared with the control group,blood sugar(26.14±3.25 mmol/L),cardiac mass index(4.03±0.39 mg/g)and left ventricular mass index(2.71±0.21 mg/g)increased significantly in the rats of diabetic model group(
P<0.05 for all)maximum rate of rise of left ventricular pressure(+dp/dt
max)and maximum rate of decrease of left ventricular pressure(-dp/dt
max)(3 852.49±86.26 and 2 336.67±55.37 mmHg)were decreased significantly(
P<0.05 for all).In addition to destroyed myocardial structure,the volume of myocardial cells were increased obviously;the levels of Ap-1,TGF-β
1 and FN were significantly up-regulated for the diabetic model group.(
P<0.05 for all).Compared with the diabetic group,blood sugar(12.83±4.31 mmol/L),cardiac mass index,and left ventricular mass index decreased for the rats in 60 mg/kg·d mangiferin group(
P<0.05 for all);the +dp/dt
max(5 236.75±71.12 mmHg/s)and -dp/dt
max(3 660.25±96.53 mmHg/s)were up-regulated(
P<0.05 for all);the volume of myocardial cells were decreased and the levels of Ap-1,TGF-β
1,and FN were also declined(
P<0.01 for all).
Conclusion Mangiferin has a protective effect on heart of diabetic rat and the mechanism may be associated with the suppression of AP-1,and the reduce of the TGF-β
1 and FN expression.