Vitamin D3 reduced helicobacter pylori infection of gastric cells by strengthening liver lipid metabolism, blocking gastric JAK-STAT3 and NF-ĸB signalling pathways and inhibiting gastric mucosal inflammation

Background: Helicobacter pylori (Hp) is a unipolar, multi-flagellate, spiral,Gram-negative bacterium that is the only stomach bacterium found in humans.Hp is the leading cause of digestive tract disease and can cause stomach diseases, such as chronic gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoma. Clinical studies have shown that Hp infection rates are significantly higher in patients with hyperlipidaemia than they are in non-hyperlipidaemic patients. In addition,many studies have shown that the serum vitamin D3 levelsare reduced in patients with obesity and hyperlipidaemia.Lower serum vitamin D3 levels diminish the role of fat cells in storing fat;as a result,fat is released into the bloodstream,leading to elevated blood lipid levels.However, a specificmechanism has not been proposed to explain how VD3 can reduce HP infection in patients with hyperlipidaemia by lowering blood lipids. Methods real-time PCR was used to detect the expression of gastrin in VDR, insign-2 and gastric tissues of mice in each group. The expression of jak, stat 3, cox2 and lkba protein in gastric tissue of mice was detected by western blotting. We also detected the expression of IL-6 and IL-8 in the gastric tissue of mice by Elisa method. The liver tissues of each group were stained with HE to observe the balloon-like changes of liver tissue, and the gastric tissues of mice in each group were stained by HE. The degree of gastritis in each group of mice. Conclusions In this article, we conducted animal experiments using VD3 as an intervention in hp-infected mice and then examined molecular changes in the VDR/Insig-2/SREBP-2 pathways in the mouse liver, the serum cholesterol levels, and the JAK-STAT3 and NF-ĸB pathways.Vitamin D3 further reduced the gastric mucosa cholesterol level,destroyed lipid rafts,and reduced assembly of IL-6 receptor subunits by lowering the circulating cholesterol levels, thereby blocking the JAK-STAT3 signalling pathway. Infection of the gastric mucosa by CagA-positive Helicobacter pylori reduced gastrin secretion and inhibited COX2 expression. Moreover, NF-κB activation and inflammatory cytokine expression were inhibited by blocking the JAK-STAT3 signalling pathway. Furthermore, the degree of infection of the gastric mucosal tissue was reduced.