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Volume 75, Issue 1, Pages 7-13 (January 2007)


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Carvedilol improved diabetic rat cardiac function depending on antioxidant ability

He HuangaCorresponding Author Informationemail addressemail address, Jiang Shanb, Xiao-Hong Panb, Hui-Ping Wangc, Ling-Bo Qianc, Qiang Xiac

Received 9 November 2005; accepted 26 April 2006. published online 16 June 2006.

Abstract 

The risk for cardiovascular disease is significantly high in diabetes mellitus. Oxidative stress plays a dominant role in the pathogenesis of diabetes mellitus. Bcl-2 gene has a close connection with antagonizing oxidative stress destroy in many diseases including diabetes. Carvedilol, an adrenoceptor blocker, also has antioxidant and free radical scavenger properties. To study the effect of carvedilol on the antioxidant status and expression of Bcl-2 in healthy and diabetic hearts, we investigated carvedilol-administrated healthy and streptozotocin-induced diabetic rats. After small and large dosage (1 or 10mg/kg/d) carvedilol-administrated for 5 weeks, hemodynamic parameters, the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and expression of Bcl-2 mRNA in the cardiac tissues of all six groups were measured. Diabetic rats had higher left ventricular end diastolic pressure (LVEDP), lower maximal rate of rise/fall left ventricle pressure development and decline (±dP/dtmax). These parameters were improved by administration of carvedilol. Diabetic rats showed elevated MDA level and CAT activity, but lower activities of SOD and GSH-Px. Carvedilol treatment increased activities of antioxidant enzymes and expression of Bcl-2 in healthy rats as well as diabetic rats. These results indicate that carvedilol improves cardiac function via its antioxidant property in diabetic rats partly.

a Department of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310016, China

b Department of Cardiology, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

c Department of Cardiovascular Physiology, Zhejiang University School of Medicine, Hangzhou, China

Corresponding Author InformationCorresponding author. Tel.: +86 571 88305110; fax: +86 571 86006242.

PII: S0168-8227(06)00171-9

doi:10.1016/j.diabres.2006.04.016


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