Effects of curcumin on gastric microvascular leakage, NF-KB-p65 expression, and change in VEGF level in Helicobacter pylori infected rats

Abstract

The H. pylori infection causes gastric inflammation and the release of inflammatory mediators. Curcumin, an active ingredient of tumeric (Curcuma longa), has many of biological activities including anti-inflammation. Therefore, this study aims to determine effects of H. pylori infection and anti-inflammatory effect of curcumin doses on the macromolecular leakage from gastric microcirculation, NF-KB-p65 expression in gastric epithelial cells and serum VEGF level in rats. Male Sprague-Dawley rats were divided into five groups including control, curcumin control, H. pylori infected, H. pylori infected with curcumin 200 mg/kg BW treated, and H. pylori infected with curcumin 600 mg/kg BW treated groups. Two weeks after H. pylori inoculation, curcumin 200 mg/kg BW or 600 mg/kg BW were fed once daily to curcumin treated group for one week. The intravital fluorescence microscopic technique was performed to examine macromolecular leakage from gastric postcapillary venules. Then, the stomach was removed for immunohistochemistry of NF-KB-p65 expression. In addition, serum VEGF was analyzed by using ELISA technique. The successful inoculation of H. pylori was 85%. H. pylori infection led to the macromolecular leakage, the NF-KB-p65 expression, and increase of VEGF level compared with control group. The average percentages of macromolecular leakage were 10.69% ± 1.43 and 15.41% ± 2.83, NF-KB-p65 immunoreactive cells were 28.58% ± 2.82 and 44.2% ± 5.24, and the average concentrations (pg/ml) of VEGF level were 228.57 ± 40.41 and 619.43 ± 145.68 in control and H. pylori infected group, respectively. Curcumin control group did not significantly change baseline of these parameters. There were significant decrease of macromolecular leakage and NF-KB-p65 expression (p ≤ 0.05) in the both curcumin treated groups compared with H. pylori infected group. The average percentages of macromolecular leakage were 12.32% ± 2.13 and 13.72% ± 2.22, and NF-KB-p65 immunoreactive cell were 33.99% ± 4.83 and 37.11% ± 4.34 in curcumin 200 and 600 mg/kg BW treated groups, respectively. Whereas, the effect of curcumin on VEGF level did not significantly change compared with H. pylori infected group. These results could be concluded that H. pylori infection increased macromolecular leakage, NF-KB-p65 expression, and serum VEGF level. Although curcumin did not significantly decrease serum VEGF level, it can reduce macromolecular leakage and NF-KB-p65 expression. It is implied that curcumin may have the anti-inflammatory effect on H. pylori infection.