No abstract

Caffeic Acid Phenethyl Ester (CAPE) is a natural compound that has been found to exhibit anti‐proliferative, anti‐inflammative, and anti‐oxidant effects, although these effects have not been fully elucidated on cardiomyocytes. Oxidative stress in the heart contributes to the pathogenesis of various cardiovascular diseases, such as ischemia/reperfusion injury following a myocardial infarction. This study investigated the cardioprotective effects of CAPE against hydrogen peroxide (H2O2)‐induced oxidative injury in rat cardiomyocytes (H9c2) in pre‐treatment (24 hours before H2O2) and co‐treatment (with H2O2), and compared these activities to vitamin C, coenzyme Q10, and caffeic acid. Cell viability was evaluated after co‐treatment and pre‐treatment by a cell counting kit‐8 assay. H2O2 (300 μM to 500 μM) dose dependently decreased cell viability, and 500 μM H2O2‐treated cells (n=4) showed a significantly decreased cell viability of 16 ± 2% compared to control cells (p<0.05). By contrast, co‐treatment (n=5) and pretreatment (n=5) of cells with CAPE (5 to 40 μM) significantly reduced cell damage in a dose dependent manner by 24–29% ± 5–8% (p<0.05). However, co‐treatment and pre‐treatment of caffeic acid (1–40 μM. n=3), vitamin C (100–10,000 μM, n=4), and coenzyme Q10 (0.1–100 μM, n=3) did not show any significant protection on cardiomyocytes against H2O2. These preliminary results suggest CAPE can protect cardiomyocytes against oxidative stress induced by H2O2, which indicate CAPE as a potentially beneficial supplement to maintain cardiovascular health. We plan to investigate the mechanism of action of CAPE in future studies.Support or Funding InformationThis study was supported by the Center for Chronic Disorders of Aging, the Division of Research and the Department of Bio‐Medical Sciences at Philadelphia College of Osteopathic Medicine.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Methylglyoxal is a precursor of advanced glycation end products which is closely related to vascular complication in diabetes. However, the direct effects of methylglyoxal on cardiac myocytes still need to be elucidated. This study investigated the dose‐dependent effects of methylglyoxal on H9C2 myoblastic cell. Furthermore, we determined if metformin would reduce methylglyoxal caused cell damage. Cell viability was evaluated by a cell counting kit‐8 assay and intracellular reactive oxygen species (ROS) was evaluated via a dichlorofluorescin diacetate (DCFDA) assay. After incubation of different doses of methylglyoxal (5 μM‐1400 μM, n=12–18) for 24 hours, lower dose range of methylglyoxal (5 μM‐800 μM) slightly increased the cell viability by 15±4% compared to the control (n=12). By contrast, higher dose methylglyoxal (1000 μM, 1200 μM, 1400 μM) significantly reduced cell viability to 74 ± 6%, 63 ± 5%, and 56 ± 7%, respectively (all p<0.05) compared to control cells. Meanwhile, higher dose of methylglyoxal (1000 μM, 1200 μM, 1400 μM) also increased intracellular ROS by 42 ± 27% (n=4), 89 ± 23% (n=4, p<0.05), and 109 ± 11% (n=3, p<0.05), respectively. By contrast, administration of metformin (1–40 mM) with methylglyoxal (1200 μM) (n=4) dose‐dependently increased cell viability. Metformin (40 mM) increased cell viability by 123± 41% (p<0.05) and reduced intracellular ROS by 70% (n=1) when compared to methylglyoxal treated cells. The preliminary data suggests that higher dose of methylglyoxal causes cardiac cells damage possibly by increased oxidative stress. Metformin can reduce oxidative stress and protect cardiac cells under higher methylglyoxal concentration and may reduce vascular complications in diabetic patients.Support or Funding InformationThis study was supported by the Center for Chronic Disorders of Aging, the Division of Research and the Department of Bio‐Medical Sciences at Philadelphia College of Osteopathic Medicine.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.