Abstract
Endotoxin, also name lipopolysaccharide (LPS), is the important pathogens of acute lung injury (ALI), which is a life-threatening diseases, which still lacking effective therapeutic strategies. Trimethyldodecatrienol, a naturally occurring sesquiterpene, has several bioeffects including anti-inflammatory, cardiprotective, neuroprotectve, and free radical scavenging effects. Pre-administration with Trimethyldodecatrienol inhibited endotoxin-induced exchange of histopathology. In addition, LPS-induced expression of proinflammatory cytokines, including tumor necrosis factor (TNF)-a, and interleukin (IL)-6, and proinflammatory mediators, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), were suppressed by trimethyldodecatrienol. The activation of nuclear factor (NF)kB, a transcription factor of proinflammatory cytokines and mediators, and degradation of IkB, which is the an inhibitor of NFkB, were also reduced by trimethyldodecatrienol. Furthermore, LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK), which including p38 MAPK, extracellular-signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) were suppressed by trimethyldodecatrienol. The inhibition of phosphorylation of MAPK occurred in the parallel with the inhibition of phosphorylation of NFkB In conclusion, trimethyldodecatrienol is a potential protective agent for ALI, possibly via down-regulating the MAPK-dependent NFkB activation pathway.
