prostaglandin-f1 has been researched along with Pancreatic-Neoplasms* in 2 studies
2 other study(ies) available for prostaglandin-f1 and Pancreatic-Neoplasms
| Article | Year |
|---|---|
Effects of selective COX-2 and 5-LOX inhibition on prostaglandin and leukotriene synthesis in ductal pancreatic cancer in Syrian hamster.
Selective inhibition of eicosanoid synthesis seems to decrease carcinogenesis, however, the effect on liver metastasis in pancreatic cancer is still unknown. Ductal pancreatic adenocarcinoma was chemically induced by weekly injection of N-nitrosobis-2-oxopropylamine (BOP) in Syrian hamster. Animals received selective inhibition of cyclooxygenase-2 (Celebrex) and 5-lipoxygenase (Zyflo). In week 33, hamsters were sacrificed and incidence of pancreatic carcinomas as well as liver metastases were examined. Furthermore, size and number of liver metastases per animal were determined and concentration of PGF1alpha, PGE2 and leukotrienes was measured in hepatic and pancreatic tissue. Combined therapy (Celebrex+Zyflo) significantly decreased incidence, number and size of liver metastases. Furthermore extra- and intrametastatic concentration of PGE2 was reduced by this treatment in hepatic tissue. Single Cox-2-inhibition (Celebrex) decreased intrametastatic hepatic PGF1alpha and PGE2 concentration while PGF1alpha concentration was reduced in non-metastatic liver (nml). Moreover 5-LOX-inhibition (Zyflo) decreased intrametastatic PGE2 concentration as well as PGF1alpha and PGE2 in nml. In pancreatic carcinomas highest LT-concentration was found after combined treatment and this therapy group was the only one revealing a significantly higher amount of LTs in carcinomas compared to tumour-free tissue. Hepatic LT-concentration was significantly lower in the control groups than in nml of the tumour groups. Combination of Cox-2-inhibition and 5-Lox-inhibition might be a suitable adjuvant therapy to prevent liver metastasis in human ductal pancreatic adenocarcinoma. Topics: Animals; Carcinoma, Pancreatic Ductal; Celecoxib; Cricetinae; Cyclooxygenase Inhibitors; Dinoprostone; Drug Therapy, Combination; Hydroxyurea; Leukotrienes; Lipoxygenase Inhibitors; Liver; Liver Neoplasms; Pancreas; Pancreatic Neoplasms; Prostaglandins; Prostaglandins F; Pyrazoles; Sulfonamides | 2005 |
Effect of prostaglandins against alloxan-induced cytotoxicity to insulin secreting insulinoma RIN cells in vitro.
In the present study, we studied the effect of various prostaglandins (PGs) on alloxan-induced cytotoxicity to rat insulinoma (RIN) cells. Of all the PGs tested, PGE(1), PGE(2), PGI(2), PGF(1 alpha), and PGF(3 alpha) protected RIN cells from alloxan-induced cytotoxicity (P<0.05 compared to alloxan), whereas thromboxane B(2) and 6-keto-PGF(1 alpha) were not effective. PGE(1) induces a statistically significant increase in the activities of superoxide dismutase and glutathione peroxidase and decrease in lipid peroxides in alloxan-treated RIN cells (P<0.001). PGE(1) restored nitric oxide/lipid peroxide ratio to normalcy, suggesting that PGE(1) suppresses oxidant stress induced by alloxan in RIN cells in vitro. Furthermore, PGE(1) prevented DNA damage and apoptosis induced by alloxan. These results indicate that PGE(1) prevents alloxan-induced cytotoxicity to RIN cells in vitro. Topics: 6-Ketoprostaglandin F1 alpha; Alloxan; Alprostadil; Animals; Antioxidants; Apoptosis; Bucladesine; Cell Death; Dinoprostone; DNA Damage; Epoprostenol; Glutathione Peroxidase; Insulin; Insulin Secretion; Insulinoma; Islets of Langerhans; Lipid Peroxides; Malondialdehyde; Nitric Oxide; Nitroprusside; Oxidative Stress; Pancreatic Neoplasms; Prostaglandins; Prostaglandins F; Rats; Superoxide Dismutase; Thromboxane B2; Tumor Cells, Cultured | 2004 |