Loganin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Response through the Activation of the Nrf2/HO-1 Signaling Pathway in RAW264.7 Macrophages

Inflammation caused by the excessive secretion of inflammatory mediators in abnormally activated macrophages promotes many diseases along with oxidative stress. Loganin, a major iridoid glycoside isolated from Cornus officinalis, has recently been reported to exhibit anti-inflammatory and antioxidant effects, whereas underlying mechanism not yet fully clarified. Therefore, aim present study is investigate effect loganin on inflammation stress lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Our results indicated that treatment markedly attenuated LPS-mediated phagocytic activity release nitric oxide (NO) prostaglandin E2, which was associated decreased expression inducible NO synthase cyclooxygenase-2. In addition, suppressed their extracellular LPS-induced pro-inflammatory cytokines, such as tumor necrosis factor-? interleukin-1?. Furthermore, abolished reactive oxygen species (ROS) generation, promoted activation nuclear factor-E2-related factor 2 (Nrf2) heme oxygenase-1 (HO-1) LPS-stimulated However, zinc protoporphyrin, selective HO-1 inhibitor, reversed loganin-mediated suppression cytokines LPS-treated conclusion, our findings suggest upregulation Nrf2/HO-1 signaling pathway concerned at least protective against stress, can be potential functional agent prevent damage.