Abstract
Tournefortia sarmentosa is a traditional Chinese medicine used to reduce tissue swelling, to exert the antioxidant effect, and to detoxify tissue. T. sarmentosa is also used to promote development in children and treat heart dysfunction. However, many of the mechanisms underlying the effects of T. sarmentosa in the treatment of disease remain unexplored. In this study, we investigated the antioxidant effect of T. sarmentosa on rat H9c2 cardiomyocytes treated with hydrogen peroxide (H2O2). T. sarmentosa reduced the cell death induced by H2O2. T. sarmentosa inhibited H2O2-induced changes in cell morphology, activation of cell death-related caspases, and production of reactive oxygen species. In addition, we further analyzed the potential active components of T. sarmentosa and found that the compounds present in the T. sarmentosa extract, including caffeic acid, rosmarinic acid, salvianolic acid A, and salvianolic acid B, exert effects similar to those of the T. sarmentosa extract in inhibiting H2O2-induced H9c2 cell death. Therefore, according to the results of this study, the ability of the T. sarmentosa extract to treat heart disease may be related to its antioxidant activity and its ability to reduce the cellular damage caused by free radicals.
Highlights
Oxidative stress caused by free radicals is associated with many cardiovascular diseases, including ischemic heart disease, atherosclerosis, hypertension, and cardiomyopathies [1,2,3,4]
H9c2 cells were selected as the experimental material and treated with 100 μM H2O2 for one hour to induce cell death as described in a previously published study in order to determine whether Reactive Oxygen Species (ROS) caused cardiomyocyte death [20]
Since T. sarmentosa inhibited the H2O2-induced death of H9c2 cells, we further explored whether T. sarmentosa altered the H2O2-induced activation of cell death-related signal transduction pathways
Summary
Oxidative stress caused by free radicals is associated with many cardiovascular diseases, including ischemic heart disease, atherosclerosis, hypertension, and cardiomyopathies [1,2,3,4]. Free radicals are generated in the human body during the process of energy production. When the body suffers from inflammation, such as inflammation elicited by infection or injury, many free radicals are produced to remove foreign substances [5]. If the host does not have a sufficient protective mechanism to remove excess free radicals after infection, these free radicals will cause cell damage (including lipid peroxidation of the cell membrane and DNA damage) [6, 7]. Environmental factors such as ultraviolet radiation, chemical drugs, and even excessive pressure result in a substantial increase in the production of free radicals in the body [8]. When cardiac muscle cells are attacked by free radicals, the free radicalsinduced injury can damage nuclear DNA and lead to permanent DNA damage. Free radicals attack the side chains of amino acids, causing proteins to lose their function and disrupting the normal functions of cells [5]
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