7th Space, 5/29/2014
Chronic inflammatory
processes in the peritoneal cavity develop as a result of ischemia, foreign
body reaction, and trauma. Brazilian green propolis, a beeswax product, has
been shown to exhibit multiple actions on inflammation and tissue repair.
Our aim was to investigate the effects of this natural
product on the inflammatory, angiogenic, and fibrogenic components of the
peritoneal fibroproliferative tissue induced by a synthetic matrix.
Methods: Chronic inflammation was induced by placing
polyether-polyurethane sponge discs in the abdominal cavity of anesthetized
Swiss mice. Oral administration of propolis (500/mg/kg/day) by gavage started
24 hours after injury for four days.
The effect of propolis on peritoneal permeability was
evaluated through fluorescein diffusion rate 4 days post implantation. The
effects of propolis on the inflammatory (myeloperoxidase and
n-acetyl-beta-D-glucosaminidase activities and TNF-alpha levels), angiogenic
(hemoglobin content-Hb), and fibrogenic (TGF-beta1 and collagen deposition)
components of the fibrovascular tissue in the implants were determined 5 days
after the injury.
Results: Propolis was able to decrease intraperitoneal
permeability. The time taken for fluorescence to peak in the systemic
circulation was 20 +/- 1 min in the treated group in contrast with 15 +/- 1 min
in the control group. In addition, the treatment was shown to down-regulate
angiogenesis (Hb content) and fibrosis by decreasing TGF-beta1 levels and
collagen deposition in fibroproliferative tissue induced by the synthetic
implants.
Conversely, the treatment up-regulated inflammatory enzyme
activities, TNF-alpha levels and gene expression of NOS2 and IFN-gamma (23 and
7 fold, respectively), and of FIZZ1 and YM1 (8 and 2 fold) when compared with the
untreated group.
Conclusions: These observations show for the first time the
effects of propolis modulating intraperitoneal inflammatory angiogenesis in
mice and disclose important action mechanisms of the compound (downregulation
of angiogenic components and activation of murine macrophage pathways).