Evaluation of the cardioprotective effect of Centella asiatica compounds.
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Univesity of the Western Cape
Abstract
Reactive oxygen species (ROS) are highly reactive and toxic by-products of cell metabolism. Biological systems are equipped with endogenous antioxidant enzymes to manage the level of ROS in the system as they can be both beneficial (for cellular redox signalling) and deleterious (involved in the initiation and progression of inflammatory diseases). In a situation where ROS production exceeds antioxidant enzyme levels, oxidative stress is experienced. This has been implicated in the initiation of atherosclerosis, which is a risk factor for coronary artery diseases and other cardiovascular-related diseases. Coronary artery disease and other related diseases are responsible for 50% of all cardiovascular diseaserelated mortalities. Hypoxia, radiation, and other factors promote the production of ROS in cardiac cells where the endogenous enzymes become overpowered. This results in the progression of cardiovascular diseases (CVDs) via various processes along the pathophysiological pathway. One of such process is the breakdown of collagen and elastin responsible for the tensile strength of heart tissue by the proteolytic enzyme cathepsin S (CatS). The approach in the past to reduce oxidative stress and the progression of oxidative stress-related CVDs has been to supplement with antioxidant molecules and biologics that mimic endogenous antioxidant enzymes like superoxide dismutase (SOD). The purpose of this study was to identify compounds from Centella asiatica with the ability to improve SOD enzyme activity, while inhibiting CatS activity, to improve CVD outcomes. Centella asiatica extracts were prepared using hexane, dichloromethane, chloroform, ethanol, ethyl acetate, methanol, acetonitrile and distilled water. The phytochemical constituents of the extracts were determined, and antioxidant activity was evaluated using the DPPH assay. The cytotoxicity of the most promising extracts (ethanol, ethyl acetate and acetonitrile) was then evaluated by MTT assay.