Inhibitory Effect of Fucoidan Combined with Bifidobacteria on Helicobacter pylori.

Fucoidan demonstrated antigastric digestive properties and promoted the growth of B. animalis BD7.

• B. animalis BD7 was characterized as gastric fluid-resistant and highly aggregative.
• Fucoidan acted as a prebiotic supporting Bifidobacterium growth under gastric conditions.
• The strain was identified as a Bifidobacterium with properties relevant to gastric survival.

The combination of FUC and B. animalis BD7 significantly inhibited the adhesion of H. pylori SS1 to gastric mucosal epithelial cells (GES-1) in vitro.

• The target cell line used was GES-1 (gastric mucosal epithelial cells).
• The H. pylori strain tested was SS1.
• Inhibition of adhesion was described as significant compared to controls.
• The combination also promoted the synthesis of bacterial inhibitory substances in vitro.

The combination of FUC and B. animalis BD7 decreased H. pylori urease activity by 71.24 ± 3.29% in vitro.

• Urease activity reduction was 71.24 ± 3.29%.
• Urease inhibition is a key metric for anti-H. pylori activity as urease is essential for bacterial survival in the gastric environment.
• This was measured in vitro alongside adhesion inhibition assays.

In vivo, the FUC and B. animalis BD7 combination alleviated gastric mucosal inflammation in H. pylori-infected mice.

• The study used a mouse model of H. pylori infection (H. pylori SS1).
• Treatment regulated the levels of inflammatory factors.
• The combination repaired the mucosal barrier in infected animals.
• Gastric mucosal inflammation was histologically or biochemically assessed.

The anti-inflammatory and mucosal protective mechanism of FUC combined with B. animalis BD7 is related to inhibition of the TLR2/MyD88/NF-κB signaling pathway.

• The TLR2/MyD88/NF-κB pathway was identified as a key mechanistic target.
• Inhibition of this pathway was associated with reduced gastric mucosal inflammation.
• This pathway is a recognized innate immune signaling cascade involved in H. pylori-induced inflammation.

The combination of FUC and B. animalis BD7 reversed gut/gastric bacterial colony disorders in H. pylori-infected mice.

• H. pylori infection caused disruption of the microbial flora, which was reversed by the combination treatment.
• Flora reversal was identified as part of the dual mechanism of action alongside TLR2/MyD88/NF-κB pathway inhibition.
• The study describes this as 'reversal of bacterial colony disorders' and 'reversal of flora disruption.'