Abstract
δ-Tocotrienol, an important component of vitamin E, has been reported to possess some physiological functions, such as anticancer and anti-inflammation, however their molecular mechanisms are not clear. In this study, δ-tocotrienol was isolated and purified from rice bran. The anti-inflammatory effect and mechanism of δ-tocotrienol against lipopolysaccharides (LPS) activated pro-inflammatory mediator expressions in RAW264.7 cells were investigated. Results showed that δ-tocotrienol significantly inhibited LPS-stimulated nitric oxide (NO) and proinflammatory cytokine (TNF-α, IFN-γ, IL-1β and IL-6) production and blocked the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinases 1/2 (ERK1/2). δ-Tocotrienol repressed the transcriptional activations and translocations of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), which were closely related with downregulated cytokine expressions. Meanwhile, δ-tocotrienol also affected the PPAR signal pathway and exerted an anti-inflammatory effect. Taken together, our data showed that δ-tocotrienol inhibited inflammation via mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor (PPAR) signalings in LPS-stimulated macrophages.
Highlights
Inflammation is a significant mechanism of the immune pathogenesis and against different harmful stimuli [1]
The yield of δ-tocotrienol that was isolated from rice bran oil that was prepared by carbon dioxide extraction was 132.7 μg/kg
We found that δ-tocotrienol inhibited mitogen-activated protein kinase (MAPK) activation and downregulated the expression of inflammatory cytokines as IL-1β, IL-6, tumor necrosis factor-α (TNF-α) and inducible NO synthase (iNOS) in the LPS-stimulated cell inflammation model
Summary
Inflammation is a significant mechanism of the immune pathogenesis and against different harmful stimuli [1]. The cellular signaling pathways and molecular mechanisms of the inflammation response are very complicated, mitogen-activated protein kinase (MAPK) is an important pathway in the initiation and development of the inflammation process. PPAR signaling can activate activator protein-1 (AP-1) and activate mitogen-activated protein kinase (MAPK) signaling, which forms a complex signal pathway net via cross-talking different pathways in the response. Δ-Tocotrienol was found to take part in a lot of health-promoting functions which include anti-diabetic, cholesterol-lowering, anticancer, antihyperlipidemic, immunomodulatory effects, antioxidant and anti-inflammation, but its molecular mechanism is not clear [26]. We used an LPS-induced macrophage inflammation model to evaluate the anti-inflammation function of δ-tocotrienol and explore if δ-tocotrienol inhibits inflammation through MAPK and PPAR pathways. We investigated the cross-talk of MAPK and PPAR pathways and how δ-tocotrienol prevented inflammation in the in vitro model
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
