Breviscapine, a traditional Chinese medicine, alleviates myocardial ischaemia reperfusion injury in diabetic rats

Abstract

Objective — The aim of this study was to explore the effects of breviscapine on the expressions of intercellular adhesion molecule-1(ICAM-1), ATPase activities and oxidative stress in ischaemia-reperfused (I/R) myocardium of diabetic rats.Methods — Sprague Dawley rats were randomly divided into two groups (a diabetic group and a non-diabetic group), and each group divided into two subgroups including a control group and a breviscapine group. Reperfusion surgery was carried out in all rats. The contents of malonaldehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in serum and myocardial tissues were measured.The activities of Na+-K+-ATPase, Mg2+-ATPase, Ca2+-ATPase in myocardial mitochondria were measured. The ICAM-1 protein expressions in myocardium were determined with the immunohistochemical method.Results — The activities of Na+-K+-ATPase, Mg2+-ATPase, Ca2+-ATPase were significantly increased in diabetic rats in the breviscapine group compared with the control group. Compared with the non-diabetic control group, the contents of MDA in serum and myocardium were significantly increased in the diabetic control group. Breviscapine led to a reduction of the contents of MDA in the diabetic and non-diabetic group. Compared with the non-diabetic control group, the activities of SOD and GSH-PX in the myocardium were significantly decreased in the diabetic control group. The activities of SOD and GSH-PX in serum and myocardium were increased in the diabetic and nondiabetic group after breviscapine treatment. Compared with the non-diabetic control group, the ICAM-1 protein expressions were increased significantly in the diabetic control group. Breviscapine decreased the ICAM-1 protein expression in the diabetic and the non-diabetic group.Conclusion — Breviscapine may have protective effects on myocardial ischaemia reperfusion injury of diabetic rats by scavenging oxygen free radicals, decreasing the expressions of ICAM-1 protein in myocardium and increasing the activities of Na+-K+-ATPase, Mg2+-ATPase, Ca2+-ATPase in myocardial mitochondria.