Breviscapine, a traditional Chinese medicine, alleviates myocardial ischaemia reperfusion injury in diabetic rats.
OBJECTIVE
The aim of this study was to explore the effects of breviscapine on the expressions of intercellular adhesion molecule-I (ICAM-I), 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-P(x)) in serum and myocardial tissues were measured. The activities of Na(+)-K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-ATPase in myocardial mitochondria were measured. The ICAM-I protein expressions in myocardium were determined with the immunohistochemical method.


RESULTS
The activities of Na(+)-K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-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-P(x) in the myocardium were significantly decreased in the diabetic control group.The activities of SOD and GSH-P(x) in serum and myocardium were increased in the diabetic and non-diabetic group after breviscapine treatment. Compared with the non-diabetic control group, the ICAM- I protein expressions were increased significantly in the diabetic control group. Breviscapine decreased the ICAM-I protein expression in the diabetic and the non-diabetic group.


CONCLUSIONS
Breviscapine may have protective effects on myocardial ischaemia reperfusion injury of diabetic rats by scavenging oxygen free radicals, decreasing the expressions of ICAM-I protein in myocardium and increasing the activities of Na(+)-K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-ATPase in myocardial mitochondria.
Jia
Jun-Hai
JH
Institute of Life Science, Jiangsu University, Zhenjiang, Jiangsu, China. junhai70@yeah.net
Chen
Ke-Ping
KP
Chen
Shu-Xian
SX
Liu
Ke-Zuo
KZ
Fan
Ting-Lu
TL
Chen
Yong-Chang
YC
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D003921:Diabetes Mellitus, Experimental; D005419:Flavonoids / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D008315:Malondialdehyde / Q000032:analysis; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D005419:Flavonoids; C061097:breviscapine; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000251:Adenosine Triphosphatases