Jaseem Saqib1, Harikesh Maurya2*
1Siddhartha Institute of Pharmacy, Near I.T. Park, Sahastradhara Road, Dehradun (UK), India
2Hygia Institute of Pharmaceutical Education and Research, Prabandh Nagar, Lucknow (UP), India
*Address for Corresponding Author
Dept. of Pharmacology,
Hygia Institute of Pharmaceutical, Education and Research, Lucknow (U.P.), India
Objective: Myocardial remodeling is the distinction of genome expression, molecular& cellular interstitial changes, and major myocardial (myocyte) that are actually responsible for changes in size, shape, heartbeat and other relevant processes includes ischemia, cell necrosis, and apoptosis. The present study was designed as the biochemical and pharmacological estimation of erythrosine in myocardial remodeling among heart failure induced by doxorubicin in the rat. Materials and Methods: Albino Wistar rats (100-150gm) were divided into 4 groups (n=6), normal control group rats were only administered with normal diet/normal saline and themyocardial remodeling were induced by a single dose of Doxorubicin (1.25mg/kg) with the association of fasting condition. The oral dose of erythrosine 0.25mg/kg and treatment drug i.e. Doxorubicin+Erythrosine were administered for the period of 16 weeks. Results: The description of the present study suggests that the CPR level (2.10±0.05 mg/dl) of erythrosine may probably control the myocardial remodeling, Creatinine level of erythrosine (0.722±0.009 mg/dl) control rat may responsible to maintain the normal myocardial function. The improvement in cholesterol (71.67±1.382 mg/dl) and triglyceride (59.50±1.746 mg/dl) levels in the treatment group may responsible for normal myocardial function. Troponin-T value (0.615±0.028 ng/ml) and CPK-MB value (593.7±5.81) of the treatment group is reported as sensitive in acute heart failure. Conclusion: Administration of Doxorubicin at single dose altered all biochemical parameters that are responsible for myocardial remodeling. From the findings of results, it is very clear that oral administration of Erythrosine may promote myocardial remodeling in the animal model.
Keywords: Myocardial remodeling, heart failure, doxorubicin, erythrosine, troponin-T