N-Acetylcysteine Decreases Myocardial Content of Inflammatory Mediators Preventing the Development of Inflammation State and Oxidative Stress in Rats Subjected to a High-Fat Diet

Scheme 1

Graphical presentation of the influence of high-fat diet (HFD) alone and combination with N-acetylcysteine (NAC) administration on the inflammation state and oxidative damage in the left ventricle tissue of rats. ↑—increase; ↓—decrease; red arrows show the effect of high-fat diet vs. control group, green arrows show the effect of NAC supplementation to rats fed an HFD vs. HFD group; phospholipase A2 (PLA2), cyclooxygenase-1, -2 (COX-1, COX-2), 5-, 12/15-lipoxygenase (5-LOX, 12/15-LOX), prostaglandin E2 (PGE2), prostaglandin I2 (PGI2), leukotriene B4, C4 (LTB4, LTC4), lipoxin A4 (LXA4), nuclear factor κB (NF-κB), tumor necrosis factor α (TNF-α), interleukin 1α (IL-1α), regulated upon activation, normal T-cell expressed and secreted (RANTES), superoxide dismutase 2 (SOD2), catalase (CAT), reduced glutathione (GSH), malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and advanced glycation end products (AGE).