Beneficial effects of Chlorella-11 peptide on blocking LPS-induced macrophage activation and alleviating thermal injury-induced inflammation in rats

Int J Immunopathol Pharmacol. Jul-Sep 2010;23(3):811-20. doi: 10.1177/039463201002300316.


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.

MeSH terms

  • Animals
  • Blotting, Western
  • Burns / complications
  • Burns / pathology*
  • Cell Line
  • Dinoprostone / biosynthesis
  • Erythema / drug therapy
  • Erythema / pathology
  • Inflammation / drug therapy*
  • Inflammation / etiology
  • Lipopolysaccharides / antagonists & inhibitors*
  • Lipopolysaccharides / toxicity
  • Macrophage Activation / drug effects*
  • Macrophages / drug effects
  • Male
  • Malondialdehyde / metabolism
  • Mice
  • NF-kappa B / biosynthesis
  • Nitric Oxide / biosynthesis
  • Nitric Oxide Synthase Type II / biosynthesis
  • Peptides / pharmacology*
  • RNA / biosynthesis
  • RNA / isolation & purification
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / blood


  • Lipopolysaccharides
  • NF-kappa B
  • Peptides
  • Tumor Necrosis Factor-alpha
  • Val-Glu-Cys-Tyr-Gly-Pro-Asn-Arg-Pro-Gln-Phe
  • Nitric Oxide
  • Malondialdehyde
  • RNA
  • Nitric Oxide Synthase Type II
  • Dinoprostone