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By clicking register, I agree to your terms. Diabetic cardiomyopathy DCM is characterized as a coronary heart disease which expands during diabetes due to alterations in the myocardial function and structure. In this experimental study, the animals were divided into three groups: The body weights of all rats were estimated at regular intervals.
The myocardial profile, oxidative stress, and activities of metabolic enzymes were also scrutinized. The proinflammatory cytokine levels together with cellular protein expression connected with apoptosis were estimated via Western blot analysis. The rats that suffered from DCM exhibited abnormal levels of myocardial markers, aberrant metabolic enzymatic activity, elevated concentrations of inflammatory factors, and enhanced oxidative stress parameters along with increased cell death apoptosis.
Whereas gingerol showed protective effects on the treated rats by an improved antioxidant defense system. The current findings suggested that gingerol is effective in the treatment of DCM by inhibition of inflammation and oxidative stress. Cardio-protective role of gingerol along with prominent anti-diabetic cardiomyopathy action in a streptozotocin-induced diabetes mellitus rat model. Introduction Diabetes mellitus DM arises by numerous etiological factors, most often via abnormal control of lipid and glycometabolism 1.
Diabetic cardiomyopathy DCM is considered a diabetes complication, which occurs due to changes in myocardial function and structure, systemic hypertension, and considered independent of coronary artery disease. An elevated concentration of free fatty acids and blood lipoproteins can expedite the expansion of cardiovascular disease, including coronary artery disease and hyperlipidemia, which able to escort the additional complications viz.
The precise mechanism of action of DCM and its etiology are unclear. Oxidative stress plays an imperative role in the expansion of the diabetic complication. Excessive generation of free radicals increases the generation of reactive oxygen species ROS and inhibits the mechanism of action of endogenous antioxidant defenses.