Abstract
Objective To demonstrat that PPARγ ligand rosiglitazone prevents gastric carcino-genesis in rats induced by chemical carcinogen N - methyl - N' - nitro - N - nitrosoguanidine (MNNG).We attempted to determinepossible anti - cancer mechanisms of rosiglitazone. Methods By examining COX -2, VEGF and MMP- 9 expression in MNNG induced gastric cancer and the rosiglitazone treated gastric cancer with RT -PCR and immunohistochemistry. Results The COX -2 and VEGF mRNA was significantly lower in rat gastric carcinoma of rosiglitazone treated group when compared with the MNNG group. Similarly, COX - 2 immunoreactivity was mainly detected in the perinuclear and cytoplasm of carci-noma cells. Expression of COX - 2 was also observed in vascular endothelial cells, fibroblasts and inflam-matory mononuclear cells in the tumor stroma. Cytoplasmic staining for VEGF was mainly seen in the tumor cells and vascular endothelial ceils, whereas COX - 2 immunostain was lower and loss of VEGF ex-pression in vascular endothelial cell was observed in rat gastric carcinoma of rosiglitazonetreated group by immunohistochemistry. Conclusions Downregulation of COX -2 and VEGF may be one of the mecha-nisms underlying the chemopreventive effect of rosighizaone in gastric cancer. Key words: Peroxisome proliferator - activated receptor - γ ; Gastric cancer; Rat model; Cycloox-ygenase -2 ; Vascular endothelial growth factor
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
