Angiotensin-I-converting enzyme (ACE) plays an important physiological role in regulation of blood pressure by converting angiotensin I to angiotensin II, a potent vasoconstrictor. Further, ACE is implicated in cell oxidative stress, augmenting the generation of ROS and peroxynitrite and also in thrombosis, during which induces platelet activation, aggregation, and adhesion (McFarlane et al., 2003). Inhibition of ACE is considered to be a useful therapeutic approach in the treatment of hypertension. Therefore, in the development of drugs to control high blood pressure, ACE inhibition has become an important activity. Many studies have been attempted in the synthesis of ACE inhibitors such as captopril, enalapril, alcacepril, and lisinopril, which are currently used in the treatment of hypertension and heart failure in human. However, these synthetic drugs are believed to have certain side effects such as cough, taste disturbances, skin rashes, or angioneurotic edema and all of which might be intrinsically linked to synthetic ACE inhibitors. The search for natural ACE inhibitors as alternatives to synthetic drugs is of great interest to prevent several side effects (Atkinson and Robertson, 1979). Fucosterol was reported as safety agent on animal models. The modulation of ACE levels was studied using fucosterol in cultured bovine carotid endothelial cells. Dexamethasone was treated to elevate the levels of ACE in the cells. After adding fucosterol to the culture medium, the activity of ACE in endothe-lial cells has decreased; however, fucosterol did not directly inhibit ACE activity. It has been found that fucosterol lowers the ACE levels in endo-thelial cells by inhibiting the synthesis of glucocorticoid receptors involved in the regulation of ACE levels (Hagiwara et al., 1986).
LDL-C is called ''bad'' cholesterol because elevated level of LDL cholesterol is associated with an increased risk of coronary heart disease. LDL lipoprotein deposits cholesterol on the artery walls, causing the formation of a hard, thick substance called cholesterol plaque. Over the time, cholesterol plaque causes thickening of the artery walls and narrowing of the arteries, a process called atherosclerosis. In contrast, HDL cholesterol is called the ''good cholesterol'' because it prevents atherosclerosis by extracting cholesterol from the artery walls and disposing them through the liver. The highest HDL-C level gives the greater capacity to remove cholesterol and prevent dangerous blockages from developing in blood vessels. HDL-C helps to keep blood vessels widened (dilated), thereby promoting better blood flow. HDL-C also reduces blood vessel injury through its antioxidant and anti-inflammatory functions, among other effects (Toth, 2005). Plant sterols have been reported as agents that can reduce the risk of heart disease by lowering LDL-C levels. Therefore, it suggested that marine algal sterols could be used to prevent cardiovascular diseases. According to Plaza et al. (2008), sterols from several edible marine algae, such as Himanthalia elongate, Undaria pinnatifida, Phorphyra spp., Chondus crispus, Cystoseira spp., Ulva spp., have potential effect on reducing the total and LDL-C level. In addition, 4-methylsterols from Crypthecodinium cohnii had no effect on any serum or liver lipid parameter. However, the percentage of serum HDL-C level was increased by 25%. Addition of bile salt to a cholesterol containing diet raises the serum and the liver cholesterol levels. Rats fed with cholesterol diet and cholesterol plus bile salt have shown significant increase in total serum cholesterol and decreased HDL-C level. Moreover, cholesterol-bile salt plus 4-methylsterols significantly raised the amount of HDL-C and triglyceride levels, but no other serum or liver lipid parameters were affected (Kritchevsky et al., 1999). These effects have shown the potential application of fucosterols in the prevention of risk of cardiovascular diseases.
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