Abstract
Chlorella possesses various remarkable biological activities. One component, Val-Glu-Cys-Tyr-Gly-Pro-Asn-Arg-Pro-Gln-Phe (Chlorella-11 peptide) was found to be able to suppress LPS-induced NO production and inflammation. However, the molecular mechanism behind these findings and the consistency between in vitro and in vivo data have not been investigated. LPS-activated RAW 264.7 macrophages were used to study in vitro molecular anti-inflammatory effects of Chlorella-11 peptide. After activation, NO production and the expression of iNOS and NF-κB proteins as well as iNOS mRNA were measured using Griess colorimetric assay, Western blotting and RT-PCR, respectively. Alterations in PGE2 and TNF-α contents were also monitored by ELISA. For in vivo studies, thermal injury Wistar rats were used and inflammatory indications e.g. serum malondialdehyde (MDA), TNF-α levels and skin erythema were evaluated 48 h after injury implementation. In vitro results showed that Chlorella-11 peptide produced a dose- and time-dependent inhibition on NO production. The effective inhibition could remain for at least 6 h after LPS activation. It was also found that the expression of LPS-induced iNOS mRNA, iNOS and NF-κB proteins were diminished by the peptide treatment. Concurrently, the levels on TNF-α and PGE2 production after LPS activation were also inhibited. These findings are in agreement with the in vivo data that animal serum MDA and TNF-α levels and skin erythema in rats were considerably reduced compared to the control group (saline-treated). The significance of this study sheds light on the effectiveness of Chlorella-11 peptide in preventing inflammation progression in vitro and in vivo and its potential for clinical applications.