Why the study?
Does orally administered rutin improve myocardial dysfunction, oxidative stress, apoptosis, and inflammation in a streptozotocin-induced diabetic rat model?
Does orally administered rutin improve myocardial dysfunction, oxidative stress, apoptosis, and inflammation in a streptozotocin-induced diabetic rat model?
In a preclinical rat model, rutin demonstrated potential therapeutic benefits for diabetic cardiomyopathy by reducing oxidative stress, inflammation, and apoptosis.
Hypothesis-generating for rutin in diabetic cardiomyopathy; prospective human trials needed before clinical adoption.
Diabetic cardiomyopathy (DCM), an independent coronary heart disease that develops in diabetic individuals, is characterized by changes in the myocardial structure and function. The aim of the present study was to investigate the protective effect of rutin on DCM in a streptozotocin-induced diabetic rat model. Rutin was orally administrated at a dose of 8 mg/kg body weight. Metabolic profiles, myocardial enzymes and oxidative stress were examined by biochemical tests. The expression levels of cellular proteins associated with apoptosis were measured by western blot analysis, while the levels of inflammatory factors were assessed by immunohistochemical analyses. Rats with DCM exhibited an abnormal metabolic profile, aberrant myocardial enzymes, elevation of oxidative stress markers, increased levels of inflammatory factors and enhanced apoptotic cell death. Notably, rutin was shown to protect and improve myocardial dysfunction, oxidative stress, apoptosis and inflammation in the hearts of the diabetic rats. In conclusion, these results indicated that rutin may have great therapeutic potential in the treatment of DCM, and possibly other cardiovascular disorders, by preventing oxidative stress, inflammation and cell death. However, further detailed studies are required to reveal the exact mechanisms underlying the protective effect of rutin.
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Wang et al. (2014) studied this question.
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