High-Density Lipoprotein Treatment Effectively Protected the Endothelial Cells, Mitochondria and Myocardium Against Oxidized Low-Density Lipoprotein Damage.

Background: This study evaluated whether high-density lipoprotein (HDL) treatment, shown to preserve endothelial cell integrity, could protect the left ventricular ejection fraction (LVEF) in rats from ischemia-reperfusion (IR) injury. Results: In vitro, protein and cellular markers of apoptosis, oxidative stress, mitochondrial damage, and MAPK-family signaling were lowest in G1, highest in G4, and significantly lower in G3 than in G2, G5, and G6 (all p < 0.0001); antioxidants and angiogenesis showed the opposite pattern. By day 28, LVEF and LV fractional shortening were highest in Group 1, lowest in Group 5, higher in Group 4 than in Groups 2, 3, and 6, and higher in Group 6 than in Groups 2 and 3 (all p < 0.0001). Inflammation, MAPK cascades, oxidative stress, mitochondrial damage, and LV infarct/fibrotic areas followed the inverse pattern, while antioxidants paralleled LVEF. Conclusions: protected heart function against IR-induced myocardial damage by inhibiting inflammation and oxidative stress and modulating MAPK-family signaling.