Corilagin (beta-1-O-galloyl-3,6-(R)-hexahydroxydiphenoyl-D-glucose) is a novel member of the
tannin family which has been discovered from many medicinal plants and has been confirmed in many pharmacological activities. However, the purified
Corilagin that was used in experiment is rare, and the anti-inflammatory mechanism of
Corilagin has not been investigated clearly. This study is to explore the inner anti-inflammatory mechanism of
Corilagin. Inflammatory cellular model was established by
lipopolysaccharide (LPS) interfering on RAW264.7 cell line. Levels of
TNF-alpha, IL-1beta,
IL-6, NO and
IL-10 in supernatant,
mRNA expression of
TNF-alpha, COX-2, iNOS and HO-1,
protein expression of COX-2 and HO-1, translocation of
NF-kappaB were assayed by ELISA or Griess method, real-time quantitative PCR, western blot and immunocytochemistry method, respectively. As a result,
Corilagin could significantly reduce production of pro-inflammatory
cytokines and mediators
TNF-alpha, IL-1beta,
IL-6, NO (iNOS) and COX-2 on both
protein and gene level by blocking
NF-kappaB nuclear translocation. Meanwhile
Corilagin could notably promote release of anti-inflammatory factor HO-1 on both
protein and gene level, but suppress the release of
IL-10. In conclusion, the anti-inflammatory effects of
Corilagin are attributed to the suppression of pro-inflammatory
cytokines and mediators by blocking
NF-kappaB activation.
Corilagin also can promote HO-1 production to induce regression of
inflammation but can inhibit
IL-10 production like
Dexamethasone.
Corilagin possesses a potential anti-inflammatory effect by not only abating inflammatory impairment but also promoting regression of
inflammation and has a good prospect to be used in many
inflammation-related diseases.