Anti-inflammatory and anti-oxidant effect of Calea urticifolia lyophilized aqueous extract on lipopolysaccharide-stimulated RAW 264.7 macrophages

Abstract

Ethnopharmacological relevanceCalea urticifolia leaves are traditionally used as a remedy to treat gastric ulcers, diabetes, and inflammation by the Xi’uy ancient native community of San Luis Potosi, Mexico. Aim of the studyThe aim was to assess the effects of the aqueous extract of the Mexican plant C. urticifolia as anti-inflammatory and anti-oxidant using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and to provide evidence on the phenolic compounds. Materials and methodsRAW 264.7 macrophages were stimulated with 1µg/mL of LPS and treated with 10, 25 50, 75 y 100µg/mL of Calea urticifolia lyophilized aqueous extract (CuAqE). Nitric oxide (NO) release, tumor necrosis factor alpha, prostaglandin E2 production, inducible nitric oxide synthase (iNOS), cyclooxygenase-2, nuclear factor-κB (NF-κB) p65, NF-κB p50 expression and reactive oxygen species (ROS) were measured; other pro-inflammatory proteins were measured with membrane antibody array. Phenolic compounds were analyzed by LC-ESI-MS. ResultsInflammation was inhibited by suppressing iNOS/NO pathway through inhibiting nucleus translocation of NF-κB p65 and p50 sub-units. ROS production was significantly (P<0.05) inhibited in a dose-dependent manner in LPS-stimulated macrophages. Moreover, the expression of inflammatory markers was suppressed (34.5–88.3%) by CuAqE. A mix of caffeoylquinic acid derivatives and flavonoid-glycosides were found in CuAqE. ConclusionPhenolic compounds in CuAqE such as caffeoylquinic acid derivatives and flavonoid glycosides could be responsible for inhibiting LPS-induced inflammation and oxidative stress by iNOS/NO pathway through suppressing NF-κB signaling pathway and by inhibition of ROS production in RAW 264.7 macrophages. Therefore, these results support the traditional knowledge of C. urticifolia tea such as an anti-inflammatory and antioxidant agent.