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Therapeutic Advances in Cardiovascular Disease 2014-Feb

Antioxidants and tumor necrosis factor alpha-inhibiting activity of sesame oil against doxorubicin-induced cardiotoxicity.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
Mohamed T S Saleem
Madhusudhana C Chetty
S Kavimani

الكلمات الدالة

نبذة مختصرة

OBJECTIVE

Oxidative stress is currently considered to be the key factor in doxorubicin-induced cardiotoxicity. Comparatively small quantity of the endogenous antioxidant content of the heart is assumed to be the predisposing factor for doxorubicin-induced cardiotoxicity. The present research was designed to evaluate the antioxidant potential and tumor necrosis factor alpha-(TNF-α) inhibiting activity of sesame oil against acute doxorubicin-induced cardiotoxicity.

METHODS

Male Wistar albino rats (180-200 g) were administered sesame oil in two dissimilar doses (5 and 10 ml/kg body weight, orally) for 30 days, followed by a single dose of doxorubicin (30 mg/kg s.c.).

RESULTS

In the doxorubicin-treated group, increased oxidative stress was proven by a significant rise of thiobarbituric acid reactive substances level and a decrease of myocardial superoxide dismutase, catalase and reduced glutathione content. Histopathological studies showed myocardial necrosis with accumulation of inflammatory cells, vacuolization and overall enlargement of the myocardium. Western blot analysis showed marked expression of TNF-α in the myocardium. Alteration in biochemical parameters by doxorubicin administration was prevented significantly (p < 0.0001) in the 5 and 10 ml/kg sesame oil treated rat hearts. Treatment with 5 and 10 ml/kg of sesame oil reduced the doxorubicin-induced TNF-α expression in the myocardium, which was associated with reduced myocyte injury. The overall effect of sesame oil was comparable with probucol, which shows similar protection.

CONCLUSIONS

The chronic oral administration of sesame oil prevents acute doxorubicin-induced cardiotoxicity by enhancing cardiac endogenous antioxidants and decreasing myocardial TNF-α expression.

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