Anti-inflammatory and anti-oxidant effect of Calea urticifolia lyophilized aqueous extract on lipopolysaccharide-stimulated RAW 264.7 macrophages
详细信息    查看全文
文摘
Calea 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 study

The 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 methods

RAW 264.7 macrophages were stimulated with 1 µg/mL of LPS and treated with 10, 25 50, 75 y 100 µg/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.

Results

Inflammation 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.

Conclusion

Phenolic 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.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700