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Diet and lifestyle play a crucial role in the progress of some cardiovascular disorders (CVDs). Rising interest in natural products and their pharmacological investigations witnessed therapeutic potential against CVDs. Caffeic acid (CA) is an organic composite hydroxycinnamic acid derivative classified among phenolics. It is a secondary metabolite biosynthesized in all plant species in the form of ester conjugates. The reported pharmacological activities of CA are neuroprotective, cardioprotective, hypoglycemic, antioxidant, and immunomodulatory properties. This work is aimed to examine the outcome of CA in atherogenic diet- (Ath-) induced rat model on lipid profile changes and endothelium function. The method involves a study duration of 35 days utilizing (n = 6) male Wistar rats (180–200 g) that were fed either normal chow or Ath. Study groups are given (i) normal chow diet, (ii) Ath, (iii) Ath + CA (25 or 50 mg/kg, p.o.), (iv) normal chow diet + CA (50 mg/kg, p.o.), and (v) Ath + Atorvastatin (ATORVA) (5 mg/kg, p.o.). Blood samples were collected at the end of the study to measure serum lipid profile, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and tissue oxidative stress level. Hemodynamic parameters and aorta staining were performed. CA treatment ameliorated lipid profile and significantly reduced the oxidative stress level. Aorta staining examination revealed a marked reduction of the atherosclerotic lesions. These findings suggested that CA is an effective treatment approach for preventing atherosclerotic lesion progression attributed to protection against oxidative stress and various enzymatic activities in the Ath model.

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Acrylamide (ACR) is an important industrial chemical agent also a food contaminant formed when food rich in carbohydrates is processed at high temperatures (120°C) such as cooking, frying, roasting, toasting, and baking. It happens when amino acid asparagine reacts with sugars, especially glucose and fructose as a result of the Maillard reaction. Its potential to cause damage to humans and animals makes it a cause for concern. After its outbreak in 2002, extensive study has been going on to prevent its formation in food. Neurological effects are by far well established for ACR along with systemic toxic effects. Diet contributes to the high proportion of ACR intake on daily basis; other exposure media are occupational, environmental, and smoking. A number of studies justifying ACR cardiotoxicity, its clear mechanism and its relevance to humans are less, but some research papers suggest the possibility of cardiotoxicity or developmental cardiotoxicity. In this review, ACR cardiac toxic effects and mechanism pathway have been discussed along with mitigation strategies.

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Objective: The relative risk of coronary heart disease in diabetic patients is more than in non-diabetic population. The present study was undertaken to explore the cardioprotective effect of Naringin on ischemia-reperfusion injury in the diabetic model of rat. Methods: Adult Wistar rats (either sex) divided into six groups. Diabetes was induced by 5 weeks combine exposure to a high-fat diet with a low dose of streptozotocin (30 mg/kg i.p.), administered on the 1st day of starting of the 5th week. Naringin treatment 25 mg/kg and 50 mg/kg was given simultaneously for 5 weeks. On the 36th day, the study animals were subjected to induction myocardial ischemia-reperfusion injury induced by the ligation of the left anterior descending coronary artery ligation in anesthetizing rat. Serum glucose level and cholesterol level measured before performing of ischemic reperfusion. After reperfusion injury, the animals were sacrificed and estimate change in the heart in the course of biochemical alterations, in creatine kinase-muscle/ brain (CK-MB) and lactate dehydrogenase, lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD) and infarct size in the heart. Results and Conclusion: Naringin treatment significantly reduced the body weight, blood glucose, cholesterol, cardiac injury biomarkers, and LPO level and increased in antioxidant (GSH and SOD) level and also significantly increased in mean arterial pressure heart rate, reduced the myocardial infarction size. The present study concludes that Naringin 50 mg/kg being more prominent action to reduce the cardiotoxicity risk in ischemia-reperfusion injury state and increases myocardial susceptibility through having more prominent antioxidant potential properties.