In this paper, to elucidate the potential mechanism by which AME and PL synergistically exerted antioxidant effects, we performed a DPPH scavenging activity-guided fractionation, and investigated the protective effect of the obtained antioxidant components against H2O2-induced oxidative damage using a MRC-5 cells model. Hypertension is the most Supercinnamaldehyde common risk factor for cardiovascular disease, stroke, and renal disease due to the elevated levels of both systolic and diastolic blood pressure. It is estimated that by the year 2025 prevalence of hypertension will be increased by 60% as compared to year 2000 and nearly 1.56 billion individuals will have hypertension worldwide. Trends in hypertension prevalence and its epidemiology in India have been critically reviewed earlier. Hypertension is responsible for 24% of all coronary heart disease deaths and 57% of all the stroke deaths in India. Essential hypertension is considered to result from the interaction of environmental and genetic factors, with approximately 30% of the inter-individual variability in blood pressure being genetically determined. The renin-angiotensinaldosterone system plays a significant role in blood pressure regulation, and has been suggested to be involved in essential hypertension. Angiotensin II receptors are of two types: type 1 GSK2981278 Receptor and type 2 receptor. Receptor binding studies provide important information regarding the distribution of AT1 and AT2 receptors and the sites of action and physiological roles of angiotensin. The peptide hormone Angiotensin II is a potent vasoconstrictor that exerts its actions through angiotensin II type 1 receptor. Essential hypertension is associated with the genetic mutations in genes of RAAS, such as the AT1R gene. Polymorphism in RAAS gene such as AT1R A1166C angiotensinogen M235T and angiotensin converting enzyme insertion/ deletion has been widely studied and found to be associated with essential hypertension. AT1R gene is composed of five exons located on chromosome 3q, where the first four exons encode the 59-untranslated region. A polymorphism in the 39 untranslated region of AT1R gene leads to the transversion of adenine to cytosine base at the 1166 position.