The mechanism of folic acid on N-methyl-N’-nitro-N-nitrosoguanidine-induced chronic atrophic gastritis through the PI3K/Akt pathway.

Abstract

Chronic atrophic gastritis (CAG) is a precancerous atrophic gastritis of the stomach, which generates an urge to develop novel therapeu-tic schedules. This study aimed to investigate the effect of experimental folic acid administration on N-methyl-N’-nitro-N-nitrosoguanidine (MNNG)-induced CAG through the PI3K/Akt pathway in rats. The rats were divided into a Model Group, a Folic Acid Group and a Blank Group. Rats in the Model Group were induced by MNNG and given 10 mL/kg/d distilled water by gavage, while rats in the Folic Acid Group were induced by MNNG and given 5 mg/kg/d folic acid suspension by gavage. As a control, rats in the Blank Group were given the same amount of distilled water as MNNG and 10 mL/kg/d distilled water by gavage. The levels of gastrin (GAS) and motilin (MTL) in serum were measured by enzyme-linked immunosorbent assay (ELISA), and the mRNA and protein ex-pressions were detected by quantitative polymerase chain reaction (q-PCR) and Western blot. According to hematoxylin and eosin (H&E) pathological analysis, there were inflammatory factors infiltration and derangement of mucosal epi-thelial cells in the model group, while the gastric tissue injury in the folic acid group was improved. Folic acid could decrease the content of GAS, increase the content of MTL in the serum of the rats, and regulate the expression of PI3K and AKT signal pathways. Folic acid can have a therapeutic effect on CAG by reducing the concentration of GAS in serum and increasing the concentration of MLT in serum. Our study would lay a theoretical foundation for using folic acid to investigate new therapies for CAG in humans.