Proinflammatory states are widely implicated in both acute and chronic disease processes. Severe acute systemic inflammation is at least partially responsible for shock and acute lung injury, and therapeutic options to curb the proinflammatory responses are limited. Sustained release of proinflammatory mediators by macrophages and other leukocyte subtypes is the hallmark of autoimmune illnesses. In addition to nonspecific immunosuppressants, targeted therapies to reduce inflammation via inhibition of cytokine release are available for some of these illnesses, including Crohn disease and rheumatoid arthritis. However, the subsequent risk of infection with these medications is significant, which limits their clinical use.
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Published online: March 04, 2013
Accepted: February 7, 2013
Received in revised form: January 29, 2013
Received: January 29, 2013
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
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- Anti-inflammatory effects of linalool in RAW 264.7 macrophages and lipopolysaccharide-induced lung injury modelJournal of Surgical ResearchVol. 180Issue 1
- PreviewInflammation, 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.