Abstract
Hyperglycemia induced advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) activation is thought to involve in the development of cardiovascular disease in diabetics. Activation of AGE-RAGE axis results in the oxidative stress and inflammation. Mangiferin is found in the bark of mango tree and is known to treat diseases owing to its various biological activities. Thus, this study was designed to evaluate the effect of mangiferin in ischemia-reperfusion (IR) induced myocardial injury in diabetic rats. A single injection of STZ (70 mg/kg; i.p.) was injected to male albino Wistar rats to induce diabetes. After confirmation of diabetes, rats were administered vehicle (2 ml/kg; i.p.) and mangiferin (40 mg/kg; i.p.) for 28 days. On 28th day, left anterior descending coronary artery was ligated for 45 min and then reperfused for 60 min. Mangiferin treatment significantly improved cardiac function, restored antioxidant status, reduced inflammation, apoptosis and maintained myocardial architecture. Furthermore, mangiferin significantly inhibited the activation of AGE-RAGE axis, c-Jun N-terminal kinase (JNK) and p38 and increased the expression of extracellular regulated kinase 1/2 (ERK1/2) in the myocardium. Thus, mangiferin attenuated IR injury in diabetic rats by modulation of AGE-RAGE/MAPK pathways which further prevented oxidative stress, inflammation and apoptosis in the myocardium.
Highlights
Contribute to the development as well as progression of various complications of diabetes including cardiomyopathy, nephropathy, retinopathy and neuropathy[8]
We demonstrated that mangiferin improved cardiac function, inhibited oxidative stress, inflammation and apoptosis in IR challenged diabetic myocardium
It has been shown that Advanced glycation end products (AGEs) production increased in the hyperglycemic state and its accumulation is responsible for worsening of IR injury in diabetics[29,30]
Summary
Contribute to the development as well as progression of various complications of diabetes including cardiomyopathy, nephropathy, retinopathy and neuropathy[8]. The direct mechanism by which glycation interferes with the cell function include denaturation of the target protein as well as decline in its function, accumulation of AGEs in tissues leading to organ malfunction, and generation of oxidative stress[9]. AGE-RAGE induced oxidative stress is involved in the pathogenesis of myocardial IR injury in diabetics; its inhibition can serve as an important means of preventing and alleviating IR injury. Mangiferin has shown to possess anti-AGE properties as mangiferin is reported to significantly ameliorate diabetic cardiomyopathy by preventing AGE-RAGE production[22]. Keeping the recent reports in mind, the present study was designed as a mechanistic approach to determine the effect of mangiferin on the myocardial IR injury in diabetic rats and further to investigate the mechanism involve in its cardioprotection
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