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-kappaB proteins as well as iNOS mRNA were measured using Griess colorimetric assay, Western blotting and RT-PCR, respectively. Alterations in PGE2 and TNF-alpha 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-alpha 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-kappaB proteins were diminished by the peptide treatment. Concurrently, the levels on TNF-alpha 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-alpha 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.
No takes yet. Share an insight, caveat, or question.
Cherng et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: