Anti-inflammatory effects of linalool in RAW 264.7 macrophages and lipopolysaccharide-induced lung injury modelInflammation, characterized by redness, swelling, pain and a sensation of heat, is one of the body’s self-defense systems. Although the inflammation response has an important role in host survival, it also leads to chronic inflammatory diseases. Linalool is a natural compound of the essential oils in several aromatic plants species. It possesses anti-inflammatory, antinociceptive, and other bioactive properties. In the present study, we investigated the protective effects of linalool on inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and an LPS-induced in vivo lung injury model.
All-trans retinoic acid preconditioning protects against liver ischemia/reperfusion injury by inhibiting the nuclear factor kappa B signaling pathwayInflammatory response plays a pathogenic role in liver ischemia/reperfusion (I/R) injury. All-trans retinoic acid (ATRA) is an active metabolite of vitamin A with anti-inflammatory effects. However, there are few reports on the anti-inflammatory effects of ATRA on liver I/R injury. The purpose of this study was to investigate the effects of ATRA on liver I/R injury and related mechanisms.
Expression of intestinal myeloid differentiation primary response protein 88 (Myd88) following experimental traumatic brain injury in a mouse modelTraumatic brain injury (TBI) can cause gastrointestinal dysfunction and increase intestinal permeability. Nuclear factor kappa B (NF-κB) has been shown to be associated with these intestinal events, but it is not well known how NF-κB is activated in the intestine after TBI. Based on previous studies, we hypothesize that myeloid differentiation primary response protein 88 (Myd88) may have an important role in NF-κB activation in the intestine, which mediates the inflammation and ultimately results in acute intestinal mucosal injury.
Milk fat globule–EGF factor VIII ameliorates liver injury after hepatic ischemia-reperfusionHepatic ischemia-reperfusion (I/R) injury is a serious clinical complication that may compromise liver function because of extensive hepatocyte loss. Therefore, the development of novel and effective therapies for hepatic I/R is critical for the improvement of patient outcome. It has been previously shown that administration of milk fat globule–EGF factor VIII (MFG-E8), a membrane-associated secretory glycoprotein, exerts significant beneficial effects under acute inflammatory conditions through multiple physiological processes associated with tissue remodeling.
Magnesium sulfate inhibits the secretion of high mobility group box 1 from lipopolysaccharide-activated RAW264.7 macrophages in vitroHigh mobility group box 1 (HMGB1) is an important inflammatory factor that is closely related to mortality in patients with sepsis. High magnesium therapy has been proved to reduce sepsis-related mortality and sepsis-induced pathologic complications. These effects result from reduced expression and release of many inflammatory cytokines, although it is not clear whether high magnesium affects the expression and release of HMGB1. In the present study, we explored the effect of magnesium sulfate on the expression and release of HMGB1 in lipopolysaccharide (LPS)-activated macrophages.
Triptolide Alleviates Hepatic Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Inhibiting NF-κB Activity in MiceHepatic I/R injury is unavoidable in liver transplantation and surgery. This remains a significant problem in surgical procedures. The purpose of this study was to investigate the effects of triptolide on liver ischemia/reperfusion (I/R) injury and related mechanisms in mice.
L-Type Calcium Channels and μ-Opioid Receptors are Involved in Mediating the Anti-Inflammatory Effects of NaloxoneWe sought to elucidate the effects of naloxone on regulating the up-regulation of inflammatory molecules and activation of the transcription factor nuclear factor-kappaB (NF-κB) induced by endotoxin. Possible roles of the μ-opioid receptors and L-type calcium channels in mediating the effects of naloxone in this regard were also investigated.