Effects of Lactobacillus plantarum B7 on serum TNF-α and IL-1β level, lipid peroxidation and apoptosis of gastric mucosa in rats infected with Helicobacter pylori

Abstract

The H. pylori infection causes gastric inflammation and the release of inflammatory mediators. L. plantarum B7 show the highest E. coli LPS-induced TNF-α inhibitory activity in vitro. The present study aims to determine anti-Helicobacter activity of L. plantarum B7 supernatants in vitro, and effects of H. pylori infection and anti-inflammatory effect of L. plantarum B7 doses on serum TNF-α and IL-1β level, histopathology of gastric mucosa, gastric malondialdehyde (MDA) level and apoptosis in gastric epithelial cells in rats. The experiments were divided into two parts. First, in vitro inhibition of H. pylori growth was examined by using L. plantarum B7 supernatants pH 4 and pH 7 at the concentration of 1X, 5X and 10X on plates that were inoculated with H. pylori. The inhibitory effect of H. pylori was interpreted by size of the inhibition zone. Secondary, male Spraque-Dawley rats were divided into four groups including control, H. pylori infected, H. pylori infected with L. plantarum B7 [superscript 6] CFUs/mL treated, and H. pylori infected with L. plantarum B7 10 [superscript 10] CFUs/mL treated groups. One week after H. pylori inoculation, L. plantarum B7 [superscript 6] CFUs/mL or 10 CFUs/mL were fed once daily to L. plantarum B7 treated groups for one week. Rats were sacrificed and blood and gastric samples were collected at the end of the study. In vitro experiment, L. plantarum B7 supernatants inhibited H. pylori growth in a dose-dependent manner and better at intact pH 4. In vivo study, in H. pylori infected group, the stomach histopathology revealed mild to moderate H. pylori colonization and inflammation. Level of gastric MDA and epithelial cell apoptosis increased significantly when compared with control group. However, there were no significant change of serum TNF-α and IL-1β level compared with control group. L. plantarum B7 treatments resulted in improving stomach pathology, decreasing of serum TNF-α level, gastric MDA level and apoptotic epithelial cells, and providing a trend of decreased IL-1β concentration. In conclusion, L. plantarum B7 could attenuate H. pylori-induced gastric inflammation by the improvement of stomach pathology, and reduction of serum TNF-α level, oxidative stress and gastric epithelial cell apoptosis. Moreover, L. plantarum B7 might have a trend to decrease IL-1β concentration. These effects might be involved in the secreted substance of L. plantarum B7 from in vitro study.