抄録
BACKGROUND
The chronic inflammatory process is a critical characteristic in several diseases. This condition has an important impact on the quality life of patients, as well as on their economic and social state. Patients in this condition use several anti-inflammatory agents, which are classified according to their chemical nature as steroidal (SAIDs) and non-steroidal (NSAIDs). However, It has been reported that its clinical use can generate dangerous adverse effects. For this motive, people use medicinal plants as an alternative of treatment. Several plants have been traditionally used as anti-inflammatory agents worldwide. One example is Psacalium decompositum, which has been reported with anti-inflammatory and antidiabetic effects. In chemical studies, sesquiterpenic compounds have been isolated, being the cacalol the main compound, which is considered the responsible principle of the anti-inflammatory effect of this plant. However, the action mechanisms involved in the anti-inflammatory action of cacalol have not yet been explored.
The aim of this investigation was to establish whether the anti-inflammatory action of cacalol involves the Nf-kB pathway, using an in vitro model.
METHODS
RAW 264.7 macrophages were cultured and pre-stimulated with LPS. Two hours after, the cells were treated with cacalol. The concentration and relative expression of cytokines were quantified by RT-PCR. The cytokines studied were TNF, IL-6, IL-1b and IL-10. The pohosphorylated subunit p65 of Nf-kB and its nuclear translocation were measured by EMSA.
RESULTS
The mRNA expression of TNF, IL-6 and IL-1b were significantly decreased in the macrophages due to cacalol. The protein concentrations in the culture of the cytokines also decreased. No changes were detected in the mRNA expression and concentration of IL-10. The cacalol decreased the concentration of the phosphorylated p65 subunit as did the translocation of Nf-kB to the nucleus.
CONCLUSIONS
Cacalol suppressed the concentrations of pro-inflammatory cytokines without affecting the anti-inflammatory cytokines. This could be associated with the inhibition of the Nf-kB pathway, since the levels of the phosphorylated p65 subunit were reduced. It is important to continue with the study of the factors involved in the regulation of said inhibition, as well as of other transcription factors involved in the anti-inflammatory action of cacalol.
